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...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 101; no. 41; pp. 14871 - 14876 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences
12.10.2004
National Acad Sciences |
Subjects | |
Online Access | Get full text |
ISSN | 0027-8424 1091-6490 |
DOI | 10.1073/pnas.0406073101 |
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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. |
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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 |
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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 |
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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 |
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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 |
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Snippet | Atherosclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in humans and experimental animals, suggests an important... |
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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 |
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