Distinct Endothelial Phenotypes Evoked by Arterial Waveforms Derived from Atherosclerosis-Susceptible and -Resistant Regions of Human Vasculature

Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in resp...

Full description

Saved in:
Bibliographic Details
Published inProceedings of the National Academy of Sciences - PNAS Vol. 101; no. 41; pp. 14871 - 14876
Main Authors Dai, Guohao, Kaazempur-Mofrad, Mohammad R., Natarajan, Sripriya, Zhang, Yuzhi, Vaughn, Saran, Blackman, Brett R., Kamm, Roger D., García-Cardeña, Guillermo, Gimbrone, Michael A.
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 12.10.2004
National Acad Sciences
Subjects
Online AccessGet full text
ISSN0027-8424
1091-6490
DOI10.1073/pnas.0406073101

Cover

Loading…
Abstract Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, "athero-prone" and "athero-protective," were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically "susceptible" or "resistant," respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of atheroprone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-κB transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries.
AbstractList Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, “athero-prone” and “athero-protective,” were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically “susceptible” or “resistant,” respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of athero-prone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-κB transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries.
Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, "athero-prone" and "athero-protective," were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically "susceptible" or "resistant," respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of athero-prone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-kappaB transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries.
Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, "athero-prone" and "athero-protective," were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically "susceptible" or "resistant," respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of athero-prone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-kappaB transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries.Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, "athero-prone" and "athero-protective," were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically "susceptible" or "resistant," respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of athero-prone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-kappaB transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries.
Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, “athero-prone” and “athero-protective,” were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically “susceptible” or “resistant,” respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of athero-prone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-κB transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries.
Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, "athero-prone" and "athero-protective," were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically "susceptible" or "resistant," respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of atheroprone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-κB transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries.
Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important role for local hemodynamic forces in atherogenesis. To explore how endothelial cells (EC) acquire functional/dysfunctional phenotypes in response to vascular region-specific flow patterns, we have used an in vitro dynamic flow system to accurately reproduce arterial shear stress waveforms on cultured human EC and have examined the effects on EC gene expression by using a high-throughput transcriptional profiling approach. The flow patterns in the carotid artery bifurcations of several normal human subjects were characterized by using 3D flow analysis based on actual vascular geometries and blood flow profiles. Two prototypic arterial waveforms, "athero-prone" and "athero-protective," were defined as representative of the wall shear stresses in two distinct regions of the carotid artery (carotid sinus and distal internal carotid artery) that are typically "susceptible" or "resistant," respectively, to atherosclerotic lesion development. These two waveforms were applied to cultured EC, and cDNA microarrays were used to analyze the differential patterns of EC gene expression. In addition, the differential effects of athero-prone vs. athero-protective waveforms were further characterized on several parameters of EC structure and function, including actin cytoskeletal organization, expression and localization of junctional proteins, activation of the NF-{kappa}B transcriptional pathway, and expression of proinflammatory cytokines and adhesion molecules. These global gene expression patterns and functional data reveal a distinct phenotypic modulation in response to the wall shear stresses present in atherosclerosis-susceptible vs. atherosclerosis-resistant human arterial geometries. [PUBLICATION ABSTRACT]
Author Natarajan, Sripriya
Zhang, Yuzhi
Kamm, Roger D.
Dai, Guohao
García-Cardeña, Guillermo
Vaughn, Saran
Gimbrone, Michael A.
Kaazempur-Mofrad, Mohammad R.
Blackman, Brett R.
AuthorAffiliation Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA 02115; and † Department of Mechanical Engineering and Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, MA 02139
AuthorAffiliation_xml – name: Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA 02115; and † Department of Mechanical Engineering and Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, MA 02139
Author_xml – sequence: 1
  givenname: Guohao
  surname: Dai
  fullname: Dai, Guohao
– sequence: 2
  givenname: Mohammad R.
  surname: Kaazempur-Mofrad
  fullname: Kaazempur-Mofrad, Mohammad R.
– sequence: 3
  givenname: Sripriya
  surname: Natarajan
  fullname: Natarajan, Sripriya
– sequence: 4
  givenname: Yuzhi
  surname: Zhang
  fullname: Zhang, Yuzhi
– sequence: 5
  givenname: Saran
  surname: Vaughn
  fullname: Vaughn, Saran
– sequence: 6
  givenname: Brett R.
  surname: Blackman
  fullname: Blackman, Brett R.
– sequence: 7
  givenname: Roger D.
  surname: Kamm
  fullname: Kamm, Roger D.
– sequence: 8
  givenname: Guillermo
  surname: García-Cardeña
  fullname: García-Cardeña, Guillermo
– sequence: 9
  givenname: Michael A.
  surname: Gimbrone
  fullname: Gimbrone, Michael A.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/15466704$$D View this record in MEDLINE/PubMed
BookMark eNqFksFu1DAQhi1URLeFMxeELA5IHNLaSZzEBw6rdqFIlUClgqPlOJOuF8debGfFPgZvjKNdtlAJcbHlme8f_TOeE3RknQWEnlNyRkldnK-tDGekJFV6UEIfoRklnGZVyckRmhGS11lT5uUxOglhRQjhrCFP0DFlZVXVpJyhn5c6RG1VxAvbubgEo6XBn5ZgXdyuIeDFxn2DDrdbPPcR_JT9KjfQOz8EfJkCm5TtvRvwPKm9C8pMpw7Z5zEoWEfdGsDSdji7gRSO0kZ8A3fa2YBdj6_GQVr8RQY1GhlHD0_R416aAM_29ym6fbe4vbjKrj--_3Axv84Uq2jMCg5F2zEGdWqYSdbknCtOGt4qlXcgGW8bWgIrm6YmHeEdqVsF6e5q2hV1cYre7squx3aAToGNXhqx9nqQfiuc1OLvjNVLcec2guU5oUXSv97rvfs-Qohi0KlfY6QFNwZRVbyqirJK4KsH4MqN3qbWxFSoScjk5uWfbg42fn9UAtgOUGm4wUMvlI4ypikmc9oISsS0EGJaCHG_EEl3_kB3KP1PBd5bmRL3NBUlFbRs6gl58x9E9KMxEX7ExL7YsasQnT_ARWo6bWnxC_NI3aU
CitedBy_id crossref_primary_10_1016_j_pcad_2007_11_003
crossref_primary_10_1152_ajpcell_00385_2007
crossref_primary_10_1002_wsbm_79
crossref_primary_10_1002_jbmr_382
crossref_primary_10_1161_ATVBAHA_111_229070
crossref_primary_10_1177_0954411920923253
crossref_primary_10_1021_ac503294p
crossref_primary_10_1038_srep12401
crossref_primary_10_3390_ijms18102034
crossref_primary_10_1093_cvr_cvs217
crossref_primary_10_1182_blood_2006_07_036020
crossref_primary_10_4330_wjc_v12_i7_303
crossref_primary_10_1155_2019_7434376
crossref_primary_10_1152_ajpheart_00719_2020
crossref_primary_10_1016_j_bbrc_2008_04_167
crossref_primary_10_1161_01_RES_0000204553_32549_a7
crossref_primary_10_1186_s40478_019_0805_4
crossref_primary_10_1152_ajpheart_00975_2011
crossref_primary_10_1161_HYPERTENSIONAHA_113_02854
crossref_primary_10_1016_j_atherosclerosis_2010_09_008
crossref_primary_10_1098_rsif_2013_0193
crossref_primary_10_1113_expphysiol_2011_059584
crossref_primary_10_1160_TH12_12_0924
crossref_primary_10_1016_j_artres_2010_05_001
crossref_primary_10_1007_s00441_008_0678_5
crossref_primary_10_1161_CIRCRESAHA_109_216283
crossref_primary_10_1007_s11883_006_0067_z
crossref_primary_10_1007_s13167_011_0064_3
crossref_primary_10_1152_ajpregu_00449_2005
crossref_primary_10_1016_j_atherosclerosis_2016_05_018
crossref_primary_10_1016_j_thromres_2010_11_021
crossref_primary_10_1016_j_yjmcc_2015_10_009
crossref_primary_10_1146_annurev_bioeng_10_061807_160521
crossref_primary_10_1161_01_RES_0000255691_76142_4a
crossref_primary_10_1002_bit_21809
crossref_primary_10_1161_ATVBAHA_108_167999
crossref_primary_10_1016_j_bbrc_2006_01_089
crossref_primary_10_1152_japplphysiol_00936_2010
crossref_primary_10_1016_j_carpath_2012_06_006
crossref_primary_10_5301_jva_5000686
crossref_primary_10_1007_s10439_010_9959_8
crossref_primary_10_1007_s10616_012_9445_2
crossref_primary_10_1002_jcp_22629
crossref_primary_10_1172_JCI135552
crossref_primary_10_1089_ars_2023_0476
crossref_primary_10_1152_ajpheart_00869_2011
crossref_primary_10_1142_S1793984413400011
crossref_primary_10_1182_blood_2010_04_278192
crossref_primary_10_1016_j_bbrc_2005_04_103
crossref_primary_10_1007_s13239_021_00518_x
crossref_primary_10_1016_j_pcad_2007_04_001
crossref_primary_10_1016_j_vph_2018_06_013
crossref_primary_10_1157_13100282
crossref_primary_10_1177_2050312120965752
crossref_primary_10_1038_s41467_017_01741_8
crossref_primary_10_1002_mrm_22325
crossref_primary_10_1227_01_NEU_0000313119_73941_9E
crossref_primary_10_1016_j_bbrc_2009_05_046
crossref_primary_10_1093_cvr_cvq115
crossref_primary_10_1152_ajpheart_00510_2009
crossref_primary_10_1161_CIRCULATIONAHA_113_001444
crossref_primary_10_1161_JAHA_112_002550
crossref_primary_10_1074_jbc_C500144200
crossref_primary_10_1146_annurev_fluid_010313_141309
crossref_primary_10_1152_ajpheart_00668_2010
crossref_primary_10_1186_1476_7120_13_1
crossref_primary_10_1186_s12944_016_0285_5
crossref_primary_10_1063_5_0076271
crossref_primary_10_1007_s11883_013_0340_x
crossref_primary_10_1161_ATVBAHA_119_313779
crossref_primary_10_1113_jphysiol_2009_172643
crossref_primary_10_1161_ATVBAHA_109_193375
crossref_primary_10_1016_j_ejmech_2020_112665
crossref_primary_10_1016_j_jbiomech_2009_09_012
crossref_primary_10_1016_j_ppedcard_2005_11_011
crossref_primary_10_1161_JAHA_112_000018
crossref_primary_10_1007_s11517_011_0735_1
crossref_primary_10_1161_CIRCULATIONAHA_105_590018
crossref_primary_10_3389_fnagi_2022_933015
crossref_primary_10_1038_labinvest_3700215
crossref_primary_10_1007_s00348_014_1832_3
crossref_primary_10_1016_j_stemcr_2013_06_007
crossref_primary_10_1111_1756_185X_12999
crossref_primary_10_1038_srep16193
crossref_primary_10_1039_c3lc50217a
crossref_primary_10_1152_ajpheart_00098_2015
crossref_primary_10_1152_physrev_00047_2009
crossref_primary_10_1038_srep39945
crossref_primary_10_1161_ATVBAHA_117_310335
crossref_primary_10_1007_s10439_010_9934_4
crossref_primary_10_1016_j_medntd_2022_100143
crossref_primary_10_1152_ajpheart_01047_2006
crossref_primary_10_1161_ATVBAHA_111_227827
crossref_primary_10_1007_s10439_018_02121_z
crossref_primary_10_1063_1_5143391
crossref_primary_10_1038_ncomms4000
crossref_primary_10_1007_s11302_014_9442_3
crossref_primary_10_1038_s41598_020_68350_2
crossref_primary_10_3389_ebm_2024_10090
crossref_primary_10_1016_j_atherosclerosis_2006_06_017
crossref_primary_10_7554_eLife_25217
crossref_primary_10_1007_s11883_023_01132_z
crossref_primary_10_1161_HYPERTENSIONAHA_112_200618
crossref_primary_10_1007_s10439_019_02371_5
crossref_primary_10_1007_s00281_007_0102_3
crossref_primary_10_1016_j_atherosclerosis_2007_03_016
crossref_primary_10_1016_j_iccl_2015_06_009
crossref_primary_10_1161_HYPERTENSIONAHA_111_00561
crossref_primary_10_3748_wjg_v23_i37_6777
crossref_primary_10_1038_s41569_019_0239_5
crossref_primary_10_1007_s10439_006_9078_8
crossref_primary_10_1016_j_arr_2017_05_006
crossref_primary_10_1016_j_cellsig_2020_109751
crossref_primary_10_7567_JJAP_56_07JF08
crossref_primary_10_1097_HJH_0000000000000777
crossref_primary_10_1016_j_devcel_2005_12_006
crossref_primary_10_1161_ATVBAHA_112_245563
crossref_primary_10_1152_ajpcell_00570_2009
crossref_primary_10_1161_ATVBAHA_114_303415
crossref_primary_10_2215_CJN_02030216
crossref_primary_10_1007_s00421_013_2684_x
crossref_primary_10_1016_j_biomaterials_2024_122686
crossref_primary_10_1515_hsz_2015_0244
crossref_primary_10_1242_dev_045351
crossref_primary_10_3389_fbioe_2019_00172
crossref_primary_10_1161_HYPERTENSIONAHA_111_183608
crossref_primary_10_1002_bit_23022
crossref_primary_10_1039_c2lc40526a
crossref_primary_10_1002_ccd_31254
crossref_primary_10_1371_journal_pone_0090213
crossref_primary_10_1115_1_4054459
crossref_primary_10_1089_ars_2015_6553
crossref_primary_10_1016_j_atherosclerosis_2016_07_930
crossref_primary_10_1161_CIRCULATIONAHA_108_805911
crossref_primary_10_1093_cvr_cvu124
crossref_primary_10_1007_s10439_005_8478_5
crossref_primary_10_1161_ATVBAHA_111_244053
crossref_primary_10_2353_ajpath_2008_071194
crossref_primary_10_1007_s13239_012_0115_5
crossref_primary_10_1126_sciadv_abl8096
crossref_primary_10_1016_j_jbiomech_2012_01_045
crossref_primary_10_1161_STROKEAHA_124_044520
crossref_primary_10_1161_CIRCRESAHA_116_308870
crossref_primary_10_1177_0192623315570340
crossref_primary_10_1093_eurheartj_ehz551
crossref_primary_10_3390_bioengineering10091036
crossref_primary_10_1039_C8NR02393J
crossref_primary_10_1103_PhysRevFluids_6_024003
crossref_primary_10_1056_NEJMra043430
crossref_primary_10_1115_1_2354211
crossref_primary_10_1038_labinvest_2009_62
crossref_primary_10_1016_j_cpcardiol_2024_102951
crossref_primary_10_1152_ajpheart_01093_2010
crossref_primary_10_1557_jmr_2006_0262
crossref_primary_10_1002_jcp_22340
crossref_primary_10_1016_j_lab_2005_12_006
crossref_primary_10_1007_s10439_005_5630_1
crossref_primary_10_1097_HCO_0b013e3282f07548
crossref_primary_10_1016_j_biopha_2008_07_053
crossref_primary_10_1007_s10237_014_0629_x
crossref_primary_10_14348_molcells_2015_0094
crossref_primary_10_3233_BIR_180205
crossref_primary_10_1038_s41392_024_01888_z
crossref_primary_10_1007_s11831_014_9142_8
crossref_primary_10_1016_j_celrep_2012_09_018
crossref_primary_10_1113_JP273255
crossref_primary_10_1007_s12170_012_0241_5
crossref_primary_10_2215_CJN_03450413
crossref_primary_10_3389_fphy_2021_636070
crossref_primary_10_1063_1_3608137
crossref_primary_10_3389_fphys_2021_785780
crossref_primary_10_1007_s12541_019_00122_z
crossref_primary_10_1152_physrev_00053_2021
crossref_primary_10_1016_j_ihj_2015_12_018
crossref_primary_10_3171_2013_12_JNS131595
crossref_primary_10_1016_j_jbc_2022_102404
crossref_primary_10_1038_s41526_022_00223_6
crossref_primary_10_1113_expphysiol_2010_056051
crossref_primary_10_1016_j_bbrc_2009_12_002
crossref_primary_10_1016_j_pharmthera_2007_10_004
crossref_primary_10_1038_sdata_2014_39
crossref_primary_10_1038_nrd1929
crossref_primary_10_1194_jlr_R400015_JLR200
crossref_primary_10_3390_ijms19030802
crossref_primary_10_1039_C7IB00065K
crossref_primary_10_1016_j_camwa_2007_08_019
crossref_primary_10_1063_5_0084600
crossref_primary_10_1016_j_biomaterials_2014_05_083
crossref_primary_10_1016_j_ijsolstr_2013_03_029
crossref_primary_10_1038_s41598_017_03532_z
crossref_primary_10_1155_2017_1515389
crossref_primary_10_1242_jcs_129437
crossref_primary_10_1042_CS20190488
crossref_primary_10_1007_s40571_022_00533_2
crossref_primary_10_1161_CIRCRESAHA_117_306457
crossref_primary_10_1097_RHU_0000000000000603
crossref_primary_10_1152_japplphysiol_00607_2021
crossref_primary_10_1083_jcb_201412052
crossref_primary_10_3390_math11040829
crossref_primary_10_1016_j_jtbi_2015_12_022
crossref_primary_10_1038_s41598_017_08982_z
crossref_primary_10_1089_scd_2016_0350
crossref_primary_10_1002_dvdy_21472
crossref_primary_10_1161_ATVBAHA_114_303425
crossref_primary_10_1152_ajpheart_00829_2010
crossref_primary_10_1227_NEU_0b013e318210f001
crossref_primary_10_1007_s10439_011_0305_6
crossref_primary_10_1115_1_2907753
crossref_primary_10_1089_ars_2006_8_1609
crossref_primary_10_1016_j_atherosclerosis_2019_07_015
crossref_primary_10_1177_2472555218761101
crossref_primary_10_3390_ijms20225694
crossref_primary_10_1016_S1885_5857_07_60154_6
crossref_primary_10_1161_CIRCULATIONAHA_120_051078
crossref_primary_10_1016_j_antiviral_2011_10_019
crossref_primary_10_1091_mbc_E16_04_0241
crossref_primary_10_1161_CIRCRESAHA_107_151860b
crossref_primary_10_1002_admi_202300137
crossref_primary_10_1007_s10439_005_9017_0
crossref_primary_10_1002_adbi_202000428
crossref_primary_10_1073_pnas_1810568115
crossref_primary_10_1136_neurintsurg_2013_010871
crossref_primary_10_1007_s10439_009_9684_3
crossref_primary_10_1038_s44161_023_00298_8
crossref_primary_10_1115_1_4001891
crossref_primary_10_1016_j_bbagen_2013_04_024
crossref_primary_10_1161_CIRCULATIONAHA_106_683227
crossref_primary_10_3390_ijms20215293
crossref_primary_10_1007_s10439_011_0313_6
crossref_primary_10_1146_annurev_pathol_1_110304_100100
crossref_primary_10_1152_physrev_00058_2009
crossref_primary_10_1042_BST0351453
crossref_primary_10_1016_j_repce_2013_07_020
crossref_primary_10_1063_1_5024386
crossref_primary_10_12688_f1000research_18901_1
crossref_primary_10_4236_jbise_2015_811073
crossref_primary_10_1113_expphysiol_2011_064006
crossref_primary_10_1016_j_jacc_2007_02_059
crossref_primary_10_1007_s13239_017_0322_1
crossref_primary_10_1186_1475_925X_8_30
crossref_primary_10_3171_2013_2_JNS12968
crossref_primary_10_1152_ajpcell_00585_2006
crossref_primary_10_1016_j_euromechflu_2012_01_010
crossref_primary_10_1083_jcb_201408103
crossref_primary_10_1096_fj_201802376RRRR
crossref_primary_10_1017_S1047951113000176
crossref_primary_10_1042_BST20200602
crossref_primary_10_1093_cvr_cvx253
crossref_primary_10_1242_jcs_138313
crossref_primary_10_1186_s13148_016_0248_8
crossref_primary_10_1016_j_freeradbiomed_2017_01_025
crossref_primary_10_1177_1087057112454741
crossref_primary_10_1016_j_mee_2018_10_010
crossref_primary_10_1016_j_bbrc_2012_02_136
crossref_primary_10_1038_ncomms2530
crossref_primary_10_1096_fj_06_8059com
crossref_primary_10_1089_ars_2010_3365
crossref_primary_10_1152_ajpheart_00708_2006
crossref_primary_10_1098_rsos_190607
crossref_primary_10_1002_jum_15253
crossref_primary_10_1016_j_isci_2023_106661
crossref_primary_10_1074_jbc_M804524200
crossref_primary_10_1097_MOL_0000000000000550
crossref_primary_10_1103_PhysRevFluids_9_083102
crossref_primary_10_1007_s10558_009_9089_9
crossref_primary_10_1080_10623320701617233
crossref_primary_10_2174_1568026623666230329085631
crossref_primary_10_1016_j_repc_2013_07_017
crossref_primary_10_1097_01_prs_0000293862_68476_97
crossref_primary_10_1016_j_atherosclerosis_2006_05_021
crossref_primary_10_1007_s11626_011_9470_z
crossref_primary_10_1016_j_bpj_2024_08_026
crossref_primary_10_1053_j_semvascsurg_2016_08_005
crossref_primary_10_1160_TH13_06_0448
crossref_primary_10_1016_j_yjmcc_2019_06_017
crossref_primary_10_1016_j_tcm_2019_01_004
crossref_primary_10_1161_JAHA_113_000134
crossref_primary_10_1152_ajpheart_01087_2006
crossref_primary_10_1371_journal_pone_0057004
crossref_primary_10_1152_ajpcell_00193_2007
crossref_primary_10_1161_CIRCRESAHA_107_152942
crossref_primary_10_5115_acb_2011_44_4_265
crossref_primary_10_1111_j_1749_6632_2012_06518_x
crossref_primary_10_1007_s10439_008_9452_9
crossref_primary_10_1016_j_vph_2023_107242
crossref_primary_10_2478_V10133_010_0066_7
crossref_primary_10_1038_nri1882
crossref_primary_10_1016_j_clim_2009_07_016
crossref_primary_10_1016_j_jbiomech_2020_109617
crossref_primary_10_1161_ATVBAHA_116_308502
crossref_primary_10_1080_13813450601094573
crossref_primary_10_1161_01_RES_0000266408_42939_e4
crossref_primary_10_1039_C5IB00199D
crossref_primary_10_1097_TP_0b013e3181e228db
crossref_primary_10_1161_STROKEAHA_109_570770
crossref_primary_10_1097_01_hjh_0000209987_51606_23
crossref_primary_10_1109_TBME_2011_2166154
crossref_primary_10_1161_01_RES_0000255690_03436_ae
crossref_primary_10_1038_s41598_025_92014_8
crossref_primary_10_3389_fphys_2018_00524
crossref_primary_10_1161_ATVBAHA_123_318964
crossref_primary_10_3389_fphar_2022_828933
crossref_primary_10_1089_ars_2012_4971
crossref_primary_10_1016_j_jtbi_2015_04_038
crossref_primary_10_1152_japplphysiol_01065_2018
crossref_primary_10_1093_cvr_cvt090
crossref_primary_10_3389_fcvm_2023_1190460
crossref_primary_10_1007_s10554_014_0571_0
crossref_primary_10_1039_C6LC00910G
crossref_primary_10_1074_jbc_M112_381509
crossref_primary_10_7554_eLife_29494
crossref_primary_10_1007_s13239_019_00426_1
crossref_primary_10_3389_fbioe_2016_00079
crossref_primary_10_1007_s12195_013_0273_z
crossref_primary_10_1111_j_1365_2265_2011_04295_x
crossref_primary_10_1093_rheumatology_ken159
crossref_primary_10_1002_biof_1137
crossref_primary_10_1016_j_ceca_2006_06_010
crossref_primary_10_18699_VJ21_062
crossref_primary_10_1042_CS20170130
crossref_primary_10_3390_ijms20215387
crossref_primary_10_1007_s13239_017_0323_0
crossref_primary_10_15829_1728_8800_2019_6_62_68
crossref_primary_10_1016_j_mtbio_2024_101121
crossref_primary_10_3389_fonc_2024_1484256
crossref_primary_10_1002_adfm_201910811
crossref_primary_10_1161_STROKEAHA_118_022322
crossref_primary_10_1002_biot_201600401
crossref_primary_10_1098_rsif_2017_0140
crossref_primary_10_1136_svn_2020_000636
crossref_primary_10_1016_j_mehy_2012_07_013
crossref_primary_10_1146_annurev_pathol_011110_130257
crossref_primary_10_1152_ajpheart_00565_2009
crossref_primary_10_1161_CIRCRESAHA_110_233841
crossref_primary_10_1016_j_ultrasmedbio_2009_09_009
crossref_primary_10_1177_1074248414555005
crossref_primary_10_1152_physrev_00014_2016
crossref_primary_10_1038_s41371_019_0273_0
crossref_primary_10_3389_fgene_2014_00422
crossref_primary_10_1007_s10544_009_9361_1
crossref_primary_10_1016_j_smim_2011_08_017
crossref_primary_10_1152_ajpheart_00079_2014
crossref_primary_10_1038_srep36461
crossref_primary_10_1093_infdis_jis200
crossref_primary_10_1161_ATVBAHA_117_310351
crossref_primary_10_1016_j_mbplus_2022_100121
crossref_primary_10_1080_07853890802186921
crossref_primary_10_1161_CIRCULATIONAHA_107_720730
crossref_primary_10_1016_j_phrs_2023_106953
crossref_primary_10_1016_j_ultrasmedbio_2024_08_017
crossref_primary_10_1016_j_vph_2012_01_007
crossref_primary_10_1073_pnas_1707517114
crossref_primary_10_1016_j_freeradbiomed_2018_01_034
crossref_primary_10_1088_0022_3727_49_49_493003
crossref_primary_10_3389_fbioe_2021_690685
crossref_primary_10_1159_000368193
crossref_primary_10_1161_ATVBAHA_117_309249
crossref_primary_10_1586_erc_10_28
crossref_primary_10_1002_wsbm_1344
crossref_primary_10_1016_j_clinbiomech_2023_105956
crossref_primary_10_1093_rheumatology_keh542
crossref_primary_10_1007_s10557_019_06863_3
crossref_primary_10_1016_j_bpj_2013_12_020
crossref_primary_10_1146_annurev_bioeng_071811_150052
crossref_primary_10_1016_j_atherosclerosis_2009_04_034
crossref_primary_10_1155_2015_354517
crossref_primary_10_1161_HYPERTENSIONAHA_110_165365
crossref_primary_10_3389_fmolb_2023_1160851
crossref_primary_10_1007_s10439_010_0145_9
crossref_primary_10_3389_fcvm_2022_955027
crossref_primary_10_1002_msj_20057
crossref_primary_10_1007_s10616_015_9941_2
crossref_primary_10_1007_s12015_006_0015_x
crossref_primary_10_1007_s13239_011_0041_y
crossref_primary_10_1002_bies_201800017
crossref_primary_10_1073_pnas_0502575102
crossref_primary_10_1161_CIRCRESAHA_108_183913
crossref_primary_10_1016_j_clim_2009_07_002
crossref_primary_10_1083_jcb_202211125
crossref_primary_10_1186_s13058_018_1071_2
crossref_primary_10_3934_mbe_2012_9_175
crossref_primary_10_1093_cvr_cvp013
crossref_primary_10_1016_j_apmt_2022_101466
crossref_primary_10_1007_s00424_013_1282_4
crossref_primary_10_1155_2017_9237263
crossref_primary_10_1038_s41598_020_64795_7
crossref_primary_10_1039_B913390A
crossref_primary_10_1126_sciadv_abg1694
crossref_primary_10_1161_ATVBAHA_109_184382
crossref_primary_10_3389_fphys_2021_621830
crossref_primary_10_1007_s11033_024_09657_5
crossref_primary_10_1093_infdis_jiq071
crossref_primary_10_1109_RBME_2024_3514378
crossref_primary_10_1039_b812184b
crossref_primary_10_1152_ajpheart_00311_2013
crossref_primary_10_1177_0271678X20910302
crossref_primary_10_1073_pnas_2122227119
crossref_primary_10_1002_jmri_20765
crossref_primary_10_1161_CIRCIMAGING_109_916304
crossref_primary_10_1016_j_biomaterials_2006_05_040
crossref_primary_10_1089_ten_teb_2023_0272
crossref_primary_10_3390_cells11193086
crossref_primary_10_1002_adhm_201901255
crossref_primary_10_1007_s10439_010_0032_4
crossref_primary_10_1016_j_compbiomed_2013_02_004
crossref_primary_10_1093_cvr_cvn360
crossref_primary_10_1115_1_4001217
crossref_primary_10_1371_journal_pone_0038590
crossref_primary_10_1007_s10439_014_1005_9
crossref_primary_10_1155_2022_2811789
crossref_primary_10_1002_adem_201080018
crossref_primary_10_1016_j_mla_2007_09_006
crossref_primary_10_1088_1758_5090_ad22ee
crossref_primary_10_1152_physrev_00004_2012
crossref_primary_10_1016_j_cellsig_2006_02_008
crossref_primary_10_1164_rccm_201210_1950ED
crossref_primary_10_1016_j_diff_2011_11_007
crossref_primary_10_1161_01_ATV_0000197858_50074_c6
crossref_primary_10_1016_j_jbiomech_2014_01_006
crossref_primary_10_4045_tidsskr_08_0011
crossref_primary_10_1016_j_compfluid_2012_12_018
crossref_primary_10_1111_j_1365_2613_2006_00506_x
crossref_primary_10_1161_CIRCRESAHA_107_168567
crossref_primary_10_1007_s10439_007_9426_3
crossref_primary_10_3109_08820139_2014_953635
crossref_primary_10_1161_ATVBAHA_109_201368
crossref_primary_10_1161_CIRCRESAHA_115_306301
crossref_primary_10_1115_1_3127248
crossref_primary_10_1016_j_atherosclerosis_2007_01_024
crossref_primary_10_1093_cvr_cvz235
crossref_primary_10_1002_adbi_201800252
crossref_primary_10_1063_1_5129812
crossref_primary_10_1016_j_purol_2016_09_052
crossref_primary_10_1161_01_ATV_0000259362_10882_c5
crossref_primary_10_1063_1_5086286
crossref_primary_10_1038_srep39553
crossref_primary_10_1016_j_ultrasmedbio_2006_07_023
crossref_primary_10_2353_ajpath_2007_060860
crossref_primary_10_1016_j_jbiomech_2011_11_012
crossref_primary_10_1073_pnas_2023236118
crossref_primary_10_1161_ATVBAHA_116_307948
crossref_primary_10_1016_j_ooc_2022_100017
crossref_primary_10_1002_btpr_2701
crossref_primary_10_14814_phy2_12171
crossref_primary_10_1152_ajpcell_00187_2012
crossref_primary_10_3389_fcell_2022_905927
crossref_primary_10_1115_1_3148191
crossref_primary_10_1016_j_plipres_2021_101142
crossref_primary_10_1016_j_yexcr_2021_112835
crossref_primary_10_1088_1758_5090_ac4fb5
crossref_primary_10_1194_jlr_R800056_JLR200
crossref_primary_10_1097_HCO_0b013e32834b7f95
crossref_primary_10_3389_fphys_2021_734215
crossref_primary_10_1227_NEU_0000000000001083
crossref_primary_10_1007_s10143_013_0501_y
crossref_primary_10_1093_eurheartj_ehu353
crossref_primary_10_1016_j_jtbi_2010_02_020
crossref_primary_10_1016_j_semnephrol_2012_02_003
crossref_primary_10_1021_acs_nanolett_5b04028
crossref_primary_10_1016_j_semnephrol_2012_02_004
crossref_primary_10_1227_01_NEU_0000298915_32248_95
Cites_doi 10.1111/j.1749-6632.2001.tb03932.x
10.1161/hq0102.104125
10.1073/pnas.96.6.3154
10.1152/ajpheart.01028.2001
10.1073/pnas.071052598
10.1016/0021-9150(87)90090-6
10.1073/pnas.93.19.10417
10.1074/jbc.M305150200
10.1073/pnas.171259298
10.1007/s10237-004-0046-7
10.1111/j.1749-6632.2001.tb03940.x
10.1115/1.2895428
10.1161/01.ATV.0000106321.63667.24
10.1056/NEJM199901143400207
10.1161/res.90.3.251
10.1182/blood-2002-01-0046
10.1074/jbc.M212897200
10.1046/j.1440-1681.2000.03297.x
10.1152/physiolgenomics.00102.2002
10.1161/01.CIR.95.4.831
10.1161/01.RES.82.5.532
10.1006/cyto.1997.0287
10.1115/1.3138276
10.1161/01.CIR.0000074223.56882.97
10.1046/j.1365-2796.1999.00564.x
10.1016/S0021-9290(97)00025-0
10.1023/B:ABME.0000032456.16097.e0
10.1161/01.CIR.0000051364.70064.D1
10.1073/pnas.97.16.9052
10.1063/1.1136909
10.1161/01.HYP.31.1.162
10.1161/01.ATV.0000105054.43931.f0
10.1161/01.ATV.5.3.293
10.1161/01.RES.86.2.114
10.1073/pnas.94.17.9314
10.1161/01.CIR.0000089373.49941.C4
10.1016/S0002-9440(10)65647-7
10.1161/01.ATV.0000083508.21989.15
10.1084/jem.20031132
10.1073/pnas.0305938101
10.1111/j.1749-6632.2000.tb06318.x
10.1114/1.140
10.1152/physiolgenomics.2001.7.1.55
10.1182/blood.V99.12.4457
10.1152/physiolgenomics.00075.2001
10.1161/01.RES.53.4.502
10.1115/1.1486468
ContentType Journal Article
Copyright Copyright 1993/2004 The National Academy of Sciences of the United States of America
Copyright National Academy of Sciences Oct 12, 2004
Copyright © 2004, The National Academy of Sciences 2004
Copyright_xml – notice: Copyright 1993/2004 The National Academy of Sciences of the United States of America
– notice: Copyright National Academy of Sciences Oct 12, 2004
– notice: Copyright © 2004, The National Academy of Sciences 2004
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7QG
7QL
7QP
7QR
7SN
7SS
7T5
7TK
7TM
7TO
7U9
8FD
C1K
FR3
H94
M7N
P64
RC3
7X8
5PM
DOI 10.1073/pnas.0406073101
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
Animal Behavior Abstracts
Bacteriology Abstracts (Microbiology B)
Calcium & Calcified Tissue Abstracts
Chemoreception Abstracts
Ecology Abstracts
Entomology Abstracts (Full archive)
Immunology Abstracts
Neurosciences Abstracts
Nucleic Acids Abstracts
Oncogenes and Growth Factors Abstracts
Virology and AIDS Abstracts
Technology Research Database
Environmental Sciences and Pollution Management
Engineering Research Database
AIDS and Cancer Research Abstracts
Algology Mycology and Protozoology Abstracts (Microbiology C)
Biotechnology and BioEngineering Abstracts
Genetics Abstracts
MEDLINE - Academic
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Virology and AIDS Abstracts
Oncogenes and Growth Factors Abstracts
Technology Research Database
Nucleic Acids Abstracts
Ecology Abstracts
Neurosciences Abstracts
Biotechnology and BioEngineering Abstracts
Environmental Sciences and Pollution Management
Entomology Abstracts
Genetics Abstracts
Animal Behavior Abstracts
Bacteriology Abstracts (Microbiology B)
Algology Mycology and Protozoology Abstracts (Microbiology C)
AIDS and Cancer Research Abstracts
Chemoreception Abstracts
Immunology Abstracts
Engineering Research Database
Calcium & Calcified Tissue Abstracts
MEDLINE - Academic
DatabaseTitleList
MEDLINE
MEDLINE - Academic

CrossRef

Virology and AIDS Abstracts
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Sciences (General)
EISSN 1091-6490
EndPage 14876
ExternalDocumentID PMC522013
791242101
15466704
10_1073_pnas_0406073101
101_41_14871
3373649
Genre Research Support, U.S. Gov't, P.H.S
Journal Article
Feature
GrantInformation_xml – fundername: NHLBI NIH HHS
  grantid: R37-HL51150
– fundername: NHLBI NIH HHS
  grantid: R01-HL61794
– fundername: NHLBI NIH HHS
  grantid: R37 HL051150
– fundername: NHLBI NIH HHS
  grantid: P50-HL56985
– fundername: NHLBI NIH HHS
  grantid: P50 HL056985
GroupedDBID ---
-DZ
-~X
.55
.GJ
0R~
123
29P
2AX
2FS
2WC
3O-
4.4
53G
5RE
5VS
85S
AACGO
AAFWJ
AANCE
AAYJJ
ABBHK
ABOCM
ABPLY
ABPPZ
ABTLG
ABXSQ
ABZEH
ACGOD
ACHIC
ACIWK
ACNCT
ACPRK
ADQXQ
ADULT
ADXHL
AENEX
AEUPB
AEXZC
AFFNX
AFOSN
AFRAH
ALMA_UNASSIGNED_HOLDINGS
AQVQM
AS~
BKOMP
CS3
D0L
DCCCD
DIK
DU5
E3Z
EBS
EJD
F5P
FRP
GX1
H13
HGD
HH5
HQ3
HTVGU
HYE
IPSME
JAAYA
JBMMH
JENOY
JHFFW
JKQEH
JLS
JLXEF
JPM
JSG
JST
KQ8
L7B
LU7
MVM
N9A
NEJ
N~3
O9-
OK1
P-O
PNE
PQQKQ
R.V
RHI
RNA
RNS
RPM
RXW
SA0
SJN
TAE
TN5
UKR
VOH
W8F
WH7
WHG
WOQ
WOW
X7M
XSW
Y6R
YBH
YKV
YSK
ZCA
ZCG
~02
~KM
-
02
0R
1AW
55
AAPBV
ABFLS
ABPTK
ADACO
ADZLD
AJYGW
AS
ASUFR
DNJUQ
DOOOF
DWIUU
DZ
F20
GJ
JSODD
KM
OHM
PQEST
RHF
VQA
X
XFK
XHC
ZA5
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7QG
7QL
7QP
7QR
7SN
7SS
7T5
7TK
7TM
7TO
7U9
8FD
C1K
FR3
H94
M7N
P64
RC3
7X8
5PM
ID FETCH-LOGICAL-c561t-39e3bd55e70915a58299c9089bcc2dea59b814e548870d09d07bce09dd71d373
ISSN 0027-8424
IngestDate Thu Aug 21 18:18:28 EDT 2025
Fri Jul 11 04:22:03 EDT 2025
Mon Jun 30 08:16:19 EDT 2025
Wed Mar 05 08:03:04 EST 2025
Tue Jul 01 03:59:58 EDT 2025
Thu Apr 24 22:51:35 EDT 2025
Wed Nov 11 00:29:30 EST 2020
Thu May 30 08:50:36 EDT 2019
Thu May 29 08:40:59 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 41
Language English
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c561t-39e3bd55e70915a58299c9089bcc2dea59b814e548870d09d07bce09dd71d373
Notes SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 14
ObjectType-Article-1
ObjectType-Feature-2
content type line 23
Abbreviations: EC, endothelial cells; OSI, oscillatory shear index; HUVEC, human umbilical vein EC; VCAM-1, vascular cell adhesion molecule 1; Cx, connexin.
Author contributions: G.D., M.R.K.-M., R.D.K., G.G.-C., and M.A.G. designed research; G.D., M.R.K.-M., Y.Z., and S.V. performed research; S.N. contributed new reagents/analytical tools; G.D., M.R.K.-M., S.N., R.D.K., G.G.-C., and M.A.G. analyzed data; G.D., G.G.-C., and M.A.G. wrote the paper; B.R.B. is one of the developers of the fluid mechanical system used in this manuscript; and M.A.G. was the principal investigator.
To whom correspondence should be addressed. E-mail: mgimbrone@rics.bwh.harvard.edu.
Present address: Department of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908.
Contributed by Michael A. Gimbrone, Jr., August 17, 2004
OpenAccessLink http://doi.org/10.1073/pnas.0406073101
PMID 15466704
PQID 201384637
PQPubID 42026
PageCount 6
ParticipantIDs crossref_citationtrail_10_1073_pnas_0406073101
jstor_primary_3373649
pubmedcentral_primary_oai_pubmedcentral_nih_gov_522013
pnas_primary_101_41_14871
proquest_journals_201384637
pubmed_primary_15466704
crossref_primary_10_1073_pnas_0406073101
proquest_miscellaneous_66966346
pnas_primary_101_41_14871_fulltext
ProviderPackageCode RNA
PNE
CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2004-10-12
PublicationDateYYYYMMDD 2004-10-12
PublicationDate_xml – month: 10
  year: 2004
  text: 2004-10-12
  day: 12
PublicationDecade 2000
PublicationPlace United States
PublicationPlace_xml – name: United States
– name: Washington
PublicationTitle Proceedings of the National Academy of Sciences - PNAS
PublicationTitleAlternate Proc Natl Acad Sci U S A
PublicationYear 2004
Publisher National Academy of Sciences
National Acad Sciences
Publisher_xml – name: National Academy of Sciences
– name: National Acad Sciences
References e_1_3_2_26_2
e_1_3_2_27_2
e_1_3_2_28_2
e_1_3_2_29_2
e_1_3_2_41_2
e_1_3_2_40_2
e_1_3_2_20_2
e_1_3_2_43_2
e_1_3_2_21_2
e_1_3_2_42_2
e_1_3_2_22_2
e_1_3_2_45_2
(e_1_3_2_10_2) 2001; 947
e_1_3_2_23_2
e_1_3_2_44_2
e_1_3_2_24_2
e_1_3_2_47_2
e_1_3_2_25_2
e_1_3_2_46_2
(e_1_3_2_4_2) 2001; 947
e_1_3_2_9_2
e_1_3_2_15_2
e_1_3_2_38_2
e_1_3_2_8_2
e_1_3_2_16_2
e_1_3_2_37_2
e_1_3_2_7_2
e_1_3_2_17_2
e_1_3_2_6_2
e_1_3_2_18_2
e_1_3_2_39_2
e_1_3_2_19_2
e_1_3_2_1_2
e_1_3_2_30_2
e_1_3_2_32_2
e_1_3_2_31_2
e_1_3_2_5_2
e_1_3_2_11_2
e_1_3_2_34_2
e_1_3_2_12_2
e_1_3_2_33_2
e_1_3_2_3_2
e_1_3_2_13_2
e_1_3_2_36_2
e_1_3_2_2_2
e_1_3_2_14_2
e_1_3_2_35_2
11795266 - Ann N Y Acad Sci. 2001 Dec;947:181-95; discussion 195-8
12003820 - Am J Physiol Heart Circ Physiol. 2002 Jun;282(6):H2124-33
10666402 - Circ Res. 2000 Feb 4;86(2):114-6
9617570 - Cytokine. 1998 Apr;10(4):258-64
11795313 - Ann N Y Acad Sci. 2001 Dec;947:93-109; discussion 109-11
9777934 - Am J Pathol. 1998 Oct;153(4):1023-33
8816815 - Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10417-22
12810612 - Circulation. 2003 Jul 1;107(25):3209-15
12738777 - J Biol Chem. 2003 Aug 8;278(32):30317-27
11296290 - Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4478-85
12963644 - Circulation. 2003 Sep 30;108(13):1619-25
7278196 - J Biomech Eng. 1981 Aug;103(3):177-85
11595792 - Physiol Genomics. 2001 Oct 10;7(1):55-63
12419857 - Physiol Genomics. 2002 Dec 26;12(1):13-23
9453297 - Hypertension. 1998 Jan;31(1 Pt 2):162-9
11948288 - Physiol Genomics. 2002;9(1):27-41
12188206 - J Biomech Eng. 2002 Aug;124(4):397-407
9054739 - Circulation. 1997 Feb 18;95(4):831-9
15136591 - J Exp Med. 2004 May 17;199(10):1305-15
9239562 - J Biomech. 1997 Aug;30(8):777-86
16273173 - Perspect Vasc Surg Endovasc Ther. 2005 Sep;17(3):268-9
11481467 - Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):8955-60
10077653 - Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):3154-9
6627609 - Circ Res. 1983 Oct;53(4):502-14
7156852 - Rev Sci Instrum. 1982 Dec;53(12):1851-4
3994585 - Arteriosclerosis. 1985 May-Jun;5(3):293-302
3689481 - Atherosclerosis. 1987 Nov;68(1-2):27-33
12958309 - J Biol Chem. 2003 Nov 21;278(47):47291-8
10901401 - Clin Exp Pharmacol Physiol. 2000 Aug;27(8):653-5
10922059 - Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9052-7
12176889 - Blood. 2002 Sep 1;100(5):1689-98
12600918 - Circulation. 2003 Feb 25;107(7):1033-9
15298431 - Ann Biomed Eng. 2004 Jul;32(7):932-46
14604830 - Arterioscler Thromb Vasc Biol. 2004 Jan;24(1):12-22
9887164 - N Engl J Med. 1999 Jan 14;340(2):115-26
15300454 - Biomech Model Mechanobiol. 2004 Sep;3(1):17-32
9846936 - Ann Biomed Eng. 1998 Nov-Dec;26(6):975-87
9256479 - Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9314-9
9529157 - Circ Res. 1998 Mar 23;82(5):532-9
12036876 - Blood. 2002 Jun 15;99(12):4457-65
11861412 - Circ Res. 2002 Feb 22;90(3):251-62
12829525 - Arterioscler Thromb Vasc Biol. 2003 Aug 1;23(8):1391-7
10865843 - Ann N Y Acad Sci. 2000 May;902:230-9; discussion 239-40
14983035 - Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2482-7
10447790 - J Intern Med. 1999 Aug;246(2):211-8
11834520 - Arterioscler Thromb Vasc Biol. 2002 Feb 1;22(2):225-30
1762445 - J Biomech Eng. 1991 Nov;113(4):464-75
14615388 - Arterioscler Thromb Vasc Biol. 2004 Jan;24(1):73-9
References_xml – volume: 947
  start-page: 93
  year: 2001
  ident: e_1_3_2_10_2
  publication-title: Ann. N.Y. Acad. Sci.
  doi: 10.1111/j.1749-6632.2001.tb03932.x
– ident: e_1_3_2_38_2
  doi: 10.1161/hq0102.104125
– ident: e_1_3_2_41_2
  doi: 10.1073/pnas.96.6.3154
– ident: e_1_3_2_42_2
  doi: 10.1152/ajpheart.01028.2001
– ident: e_1_3_2_11_2
  doi: 10.1073/pnas.071052598
– ident: e_1_3_2_6_2
  doi: 10.1016/0021-9150(87)90090-6
– ident: e_1_3_2_36_2
  doi: 10.1073/pnas.93.19.10417
– ident: e_1_3_2_25_2
  doi: 10.1074/jbc.M305150200
– ident: e_1_3_2_12_2
  doi: 10.1073/pnas.171259298
– ident: e_1_3_2_20_2
  doi: 10.1007/s10237-004-0046-7
– volume: 947
  start-page: 181
  year: 2001
  ident: e_1_3_2_4_2
  publication-title: Ann. N.Y. Acad. Sci.
  doi: 10.1111/j.1749-6632.2001.tb03940.x
– ident: e_1_3_2_19_2
  doi: 10.1115/1.2895428
– ident: e_1_3_2_46_2
  doi: 10.1161/01.ATV.0000106321.63667.24
– ident: e_1_3_2_1_2
  doi: 10.1056/NEJM199901143400207
– ident: e_1_3_2_30_2
  doi: 10.1161/res.90.3.251
– ident: e_1_3_2_33_2
  doi: 10.1182/blood-2002-01-0046
– ident: e_1_3_2_31_2
  doi: 10.1074/jbc.M212897200
– ident: e_1_3_2_32_2
  doi: 10.1046/j.1440-1681.2000.03297.x
– ident: e_1_3_2_14_2
  doi: 10.1152/physiolgenomics.00102.2002
– ident: e_1_3_2_28_2
  doi: 10.1161/01.CIR.95.4.831
– ident: e_1_3_2_26_2
  doi: 10.1161/01.RES.82.5.532
– ident: e_1_3_2_44_2
  doi: 10.1006/cyto.1997.0287
– ident: e_1_3_2_23_2
  doi: 10.1115/1.3138276
– ident: e_1_3_2_29_2
  doi: 10.1161/01.CIR.0000074223.56882.97
– ident: e_1_3_2_39_2
  doi: 10.1046/j.1365-2796.1999.00564.x
– ident: e_1_3_2_18_2
  doi: 10.1016/S0021-9290(97)00025-0
– ident: e_1_3_2_21_2
  doi: 10.1023/B:ABME.0000032456.16097.e0
– ident: e_1_3_2_40_2
  doi: 10.1161/01.CIR.0000051364.70064.D1
– ident: e_1_3_2_45_2
  doi: 10.1073/pnas.97.16.9052
– ident: e_1_3_2_22_2
  doi: 10.1063/1.1136909
– ident: e_1_3_2_9_2
  doi: 10.1161/01.HYP.31.1.162
– ident: e_1_3_2_2_2
  doi: 10.1161/01.ATV.0000105054.43931.f0
– ident: e_1_3_2_5_2
  doi: 10.1161/01.ATV.5.3.293
– ident: e_1_3_2_8_2
  doi: 10.1161/01.RES.86.2.114
– ident: e_1_3_2_37_2
  doi: 10.1073/pnas.94.17.9314
– ident: e_1_3_2_47_2
  doi: 10.1161/01.CIR.0000089373.49941.C4
– ident: e_1_3_2_3_2
  doi: 10.1016/S0002-9440(10)65647-7
– ident: e_1_3_2_43_2
  doi: 10.1161/01.ATV.0000083508.21989.15
– ident: e_1_3_2_34_2
  doi: 10.1084/jem.20031132
– ident: e_1_3_2_35_2
  doi: 10.1073/pnas.0305938101
– ident: e_1_3_2_7_2
  doi: 10.1111/j.1749-6632.2000.tb06318.x
– ident: e_1_3_2_24_2
  doi: 10.1114/1.140
– ident: e_1_3_2_13_2
  doi: 10.1152/physiolgenomics.2001.7.1.55
– ident: e_1_3_2_27_2
  doi: 10.1182/blood.V99.12.4457
– ident: e_1_3_2_15_2
  doi: 10.1152/physiolgenomics.00075.2001
– ident: e_1_3_2_16_2
  doi: 10.1161/01.RES.53.4.502
– ident: e_1_3_2_17_2
  doi: 10.1115/1.1486468
– reference: 1762445 - J Biomech Eng. 1991 Nov;113(4):464-75
– reference: 11595792 - Physiol Genomics. 2001 Oct 10;7(1):55-63
– reference: 9054739 - Circulation. 1997 Feb 18;95(4):831-9
– reference: 9256479 - Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9314-9
– reference: 9777934 - Am J Pathol. 1998 Oct;153(4):1023-33
– reference: 7156852 - Rev Sci Instrum. 1982 Dec;53(12):1851-4
– reference: 12188206 - J Biomech Eng. 2002 Aug;124(4):397-407
– reference: 12419857 - Physiol Genomics. 2002 Dec 26;12(1):13-23
– reference: 11948288 - Physiol Genomics. 2002;9(1):27-41
– reference: 9239562 - J Biomech. 1997 Aug;30(8):777-86
– reference: 12958309 - J Biol Chem. 2003 Nov 21;278(47):47291-8
– reference: 14983035 - Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2482-7
– reference: 15298431 - Ann Biomed Eng. 2004 Jul;32(7):932-46
– reference: 12003820 - Am J Physiol Heart Circ Physiol. 2002 Jun;282(6):H2124-33
– reference: 11481467 - Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):8955-60
– reference: 12036876 - Blood. 2002 Jun 15;99(12):4457-65
– reference: 11296290 - Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4478-85
– reference: 12176889 - Blood. 2002 Sep 1;100(5):1689-98
– reference: 14615388 - Arterioscler Thromb Vasc Biol. 2004 Jan;24(1):73-9
– reference: 11834520 - Arterioscler Thromb Vasc Biol. 2002 Feb 1;22(2):225-30
– reference: 15300454 - Biomech Model Mechanobiol. 2004 Sep;3(1):17-32
– reference: 10666402 - Circ Res. 2000 Feb 4;86(2):114-6
– reference: 14604830 - Arterioscler Thromb Vasc Biol. 2004 Jan;24(1):12-22
– reference: 12810612 - Circulation. 2003 Jul 1;107(25):3209-15
– reference: 12829525 - Arterioscler Thromb Vasc Biol. 2003 Aug 1;23(8):1391-7
– reference: 10077653 - Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):3154-9
– reference: 10447790 - J Intern Med. 1999 Aug;246(2):211-8
– reference: 10901401 - Clin Exp Pharmacol Physiol. 2000 Aug;27(8):653-5
– reference: 11795266 - Ann N Y Acad Sci. 2001 Dec;947:181-95; discussion 195-8
– reference: 3994585 - Arteriosclerosis. 1985 May-Jun;5(3):293-302
– reference: 16273173 - Perspect Vasc Surg Endovasc Ther. 2005 Sep;17(3):268-9
– reference: 10865843 - Ann N Y Acad Sci. 2000 May;902:230-9; discussion 239-40
– reference: 12600918 - Circulation. 2003 Feb 25;107(7):1033-9
– reference: 3689481 - Atherosclerosis. 1987 Nov;68(1-2):27-33
– reference: 11861412 - Circ Res. 2002 Feb 22;90(3):251-62
– reference: 9453297 - Hypertension. 1998 Jan;31(1 Pt 2):162-9
– reference: 10922059 - Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9052-7
– reference: 9617570 - Cytokine. 1998 Apr;10(4):258-64
– reference: 9529157 - Circ Res. 1998 Mar 23;82(5):532-9
– reference: 12738777 - J Biol Chem. 2003 Aug 8;278(32):30317-27
– reference: 9887164 - N Engl J Med. 1999 Jan 14;340(2):115-26
– reference: 15136591 - J Exp Med. 2004 May 17;199(10):1305-15
– reference: 6627609 - Circ Res. 1983 Oct;53(4):502-14
– reference: 11795313 - Ann N Y Acad Sci. 2001 Dec;947:93-109; discussion 109-11
– reference: 9846936 - Ann Biomed Eng. 1998 Nov-Dec;26(6):975-87
– reference: 12963644 - Circulation. 2003 Sep 30;108(13):1619-25
– reference: 7278196 - J Biomech Eng. 1981 Aug;103(3):177-85
– reference: 8816815 - Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10417-22
SSID ssj0009580
Score 2.3809187
Snippet Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important...
SourceID pubmedcentral
proquest
pubmed
crossref
pnas
jstor
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 14871
SubjectTerms Arteriosclerosis - genetics
Arteriosclerosis - pathology
Atherosclerosis
Biological Sciences
Blood Flow Velocity
Carotid arteries
Carotid Arteries - physiology
Carotid sinus
Cells
Cytoskeletal Proteins - genetics
Disease Susceptibility
Drug therapy
Endothelium, Vascular - pathology
Endothelium, Vascular - physiology
Gene expression
Gene Expression Regulation
Genes
Genotype & phenotype
Hemodynamics
Humans
Immunity, Innate
Lesions
Phenotypes
Regional Blood Flow
Shear stress
Waveform analysis
Waveforms
Title Distinct Endothelial Phenotypes Evoked by Arterial Waveforms Derived from Atherosclerosis-Susceptible and -Resistant Regions of Human Vasculature
URI https://www.jstor.org/stable/3373649
http://www.pnas.org/content/101/41/14871.abstract
https://www.ncbi.nlm.nih.gov/pubmed/15466704
https://www.proquest.com/docview/201384637
https://www.proquest.com/docview/66966346
https://pubmed.ncbi.nlm.nih.gov/PMC522013
Volume 101
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFLa28cILYjAgjIuFeBiqUpqb3T5ObGNCW9lDJ5WnyE4ctdAmU5MObf-Cf8w5tpO0Y5uAl7SN3Tjt-XJuPhdC3icAWk_5kRspn4GBkoWuiDLuSj-LWF96fS7RD3k6ZMfn4ZdxNN7Y3FyJWlpWsptc35pX8j9UhXNAV8yS_QfKNheFE_Ae6AtHoDAc_4rGB_iA5knVUXmKmVQzdH9j0FaBntWyoy6LH0bD1JGbOPpTXCrUU8tOCicuYVQnmGg9sCjh-nCclm65LHW8C-ZV6RYaYJWjpplXHWzlYIPnTIM_G8xa1yapVd2zRjSWdSDCsPY87rd5LJa5lB23czZsuyIfmDbZhzMAcTERRSMYhLhW84vlwj0tsoXB5ylMmM9F2gY_wkJiIb5b5y7wxcX0qpE_jY_82_J6Ml1ze4SujiJpo0LuueFVfu-DDA5NlnZXGRYPGpLLQtOktJEB1qNiwG5KcVmWDvaiaRLzh7AB7ogdknNRdoEVMvhYX2atrPfwa3x0fnISjw7Ho_VRrUbwgYfb8piD-MAHWwfbcHweeyuVo_smj8r-lLo-FQ8-3lh6TbUy0bVYshcm3WY-3YwCXlGrRo_JI2sP0X0D7m2yofInZLv-j-meLYv-4Sn5VaOdrqCdtminBu1UXtEa7bRBO7Vop4h2eg_aKaCdtminFu20yKhGO11B-w4ZHR2OPh27tqGIm4CZULnBQAUyjSLFAQORiPqgiyW48S2TxE-ViAay74UKjHiQYmlvkPa4TBS8ptxLAx48I1t5kasXhEaSJzzwB0nWS3ArXaSh8HgmPYkSkvkO6dakiBNbbB97vsxiHfTBgxjJEre0c8he84ULU2fm7qk7mrbNvABuDQDtEEfPbL_uxaEXa_w65N2dY3Fmw8wcslujJLZcrox9DGUIWcAd8rYZBRGE-4oiV8WyjBkbgN0SMoc8N4hql4lCxngvdAhbw1ozAYvbr4_k04kucg92Iaz88t5b2iUPW9bwimxVi6V6DTZCJd_oZ-g3Z9Ea6w
linkProvider Geneva Foundation for Medical Education and Research
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Distinct+endothelial+phenotypes+evoked+by+arterial+waveforms+derived+from+atherosclerosis-susceptible+and+-resistant+regions+of+human+vasculature&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+-+PNAS&rft.au=Dai%2C+El+Guohao&rft.au=Kaazempur-Mofrad%2C+Mohammad+R&rft.au=Natarajan%2C+Sripriya&rft.au=Zhang%2C+Yuzhi&rft.date=2004-10-12&rft.pub=National+Academy+of+Sciences&rft.issn=0027-8424&rft.eissn=1091-6490&rft.volume=101&rft.issue=41&rft.spage=14871&rft_id=info:doi/10.1073%2Fpnas.0406073101&rft.externalDBID=NO_FULL_TEXT&rft.externalDocID=791242101
thumbnail_m http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=http%3A%2F%2Fwww.pnas.org%2Fcontent%2F101%2F41.cover.gif
thumbnail_s http://utb.summon.serialssolutions.com/2.0.0/image/custom?url=http%3A%2F%2Fwww.pnas.org%2Fcontent%2F101%2F41.cover.gif