Mechanistic Role of the Calcium-Dependent Protease Calpain in the Endothelial Dysfunction Induced by MPO (Myeloperoxidase)
MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. The molecular mechanisms of the endothelial damaging action of MPO remain though largely elusive. Calpain is a calcium-d...
Saved in:
Published in | Hypertension (Dallas, Tex. 1979) Vol. 71; no. 4; pp. 761 - 770 |
---|---|
Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Heart Association, Inc
01.04.2018
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. The molecular mechanisms of the endothelial damaging action of MPO remain though largely elusive. Calpain is a calcium-dependent protease expressed in the vascular wall. Activation of calpains has been implicated in inflammatory disorders of the vasculature. Using endothelial cells and genetically modified mice, this study identifies the µ-calpain isoform as novel downstream signaling target of MPO in endothelial dysfunction. Mouse lung microvascular endothelial cells were stimulated with 10 nmol/L MPO for 180 minutes. MPO denitrosylated µ-calpain C-terminus domain, and time dependently activated µ-calpain, but not the m-calpain isoform. MPO also reduced Thr AMPK (AMP-activated protein kinase) and Ser eNOS (endothelial nitric oxide synthase) phosphorylation via upregulation of PP2A (protein phosphatase 2) expression. At the functional level, MPO increased endothelial VCAM-1 (vascular cell adhesion molecule 1) abundance and the adhesion of leukocytes to the mouse aorta. In MPO-treated endothelial cells, pharmacological inhibition of calpain activity attenuated expression of VCAM-1 and PP2A, and restored Thr AMPK and Ser eNOS phosphorylation. Compared with wild-type mice, µ-calpain deficient mice experienced reduced leukocyte adhesion to the aortic endothelium in response to MPO. Our data first establish a role for calpain in the endothelial dysfunction and vascular inflammation of MPO. The MPO/calpain/PP2A signaling pathway may provide novel pharmacological targets for the treatment of inflammatory vascular disorders. |
---|---|
AbstractList | MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. The molecular mechanisms of the endothelial damaging action of MPO remain though largely elusive. Calpain is a calcium-dependent protease expressed in the vascular wall. Activation of calpains has been implicated in inflammatory disorders of the vasculature. Using endothelial cells and genetically modified mice, this study identifies the µ-calpain isoform as novel downstream signaling target of MPO in endothelial dysfunction. Mouse lung microvascular endothelial cells were stimulated with 10 nmol/L MPO for 180 minutes. MPO denitrosylated µ-calpain C-terminus domain, and time dependently activated µ-calpain, but not the m-calpain isoform. MPO also reduced Thr172 AMPK (AMP-activated protein kinase) and Ser1177 eNOS (endothelial nitric oxide synthase) phosphorylation via upregulation of PP2A (protein phosphatase 2) expression. At the functional level, MPO increased endothelial VCAM-1 (vascular cell adhesion molecule 1) abundance and the adhesion of leukocytes to the mouse aorta. In MPO-treated endothelial cells, pharmacological inhibition of calpain activity attenuated expression of VCAM-1 and PP2A, and restored Thr172 AMPK and Ser1177 eNOS phosphorylation. Compared with wild-type mice, µ-calpain deficient mice experienced reduced leukocyte adhesion to the aortic endothelium in response to MPO. Our data first establish a role for calpain in the endothelial dysfunction and vascular inflammation of MPO. The MPO/calpain/PP2A signaling pathway may provide novel pharmacological targets for the treatment of inflammatory vascular disorders. MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. The molecular mechanisms of the endothelial damaging action of MPO remain though largely elusive. Calpain is a calcium-dependent protease expressed in the vascular wall. Activation of calpains has been implicated in inflammatory disorders of the vasculature. Using endothelial cells and genetically modified mice, this study identifies the µ-calpain isoform as novel downstream signaling target of MPO in endothelial dysfunction. Mouse lung microvascular endothelial cells were stimulated with 10 nmol/L MPO for 180 minutes. MPO denitrosylated µ-calpain C-terminus domain, and time dependently activated µ-calpain, but not the m-calpain isoform. MPO also reduced Thr AMPK (AMP-activated protein kinase) and Ser eNOS (endothelial nitric oxide synthase) phosphorylation via upregulation of PP2A (protein phosphatase 2) expression. At the functional level, MPO increased endothelial VCAM-1 (vascular cell adhesion molecule 1) abundance and the adhesion of leukocytes to the mouse aorta. In MPO-treated endothelial cells, pharmacological inhibition of calpain activity attenuated expression of VCAM-1 and PP2A, and restored Thr AMPK and Ser eNOS phosphorylation. Compared with wild-type mice, µ-calpain deficient mice experienced reduced leukocyte adhesion to the aortic endothelium in response to MPO. Our data first establish a role for calpain in the endothelial dysfunction and vascular inflammation of MPO. The MPO/calpain/PP2A signaling pathway may provide novel pharmacological targets for the treatment of inflammatory vascular disorders. MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. The molecular mechanisms of the endothelial damaging action of MPO remain though largely elusive. Calpain is a calcium-dependent protease expressed in the vascular wall. Activation of calpains has been implicated in inflammatory disorders of the vasculature. Using endothelial cells and genetically modified mice, this study identifies the µ-calpain isoform as novel downstream signaling target of MPO in endothelial dysfunction. Mouse lung microvascular endothelial cells were stimulated with 10 nmol/L MPO for 180 minutes. MPO denitrosylated µ-calpain C-terminus domain, and time dependently activated µ-calpain, but not the m-calpain isoform. MPO also reduced Thr 172 AMPK (AMP-activated protein kinase) and Ser 1177 eNOS (endothelial nitric oxide synthase) phosphorylation via upregulation of PP2A (protein phosphatase 2) expression. At the functional level, MPO increased endothelial VCAM-1 (vascular cell adhesion molecule 1) abundance and the adhesion of leukocytes to the mouse aorta. In MPO-treated endothelial cells, pharmacological inhibition of calpain activity attenuated expression of VCAM-1 and PP2A, and restored Thr 172 AMPK and Ser 1177 eNOS phosphorylation. Compared with wild-type mice, µ-calpain deficient mice experienced reduced leukocyte adhesion to the aortic endothelium in response to MPO. Our data first establish a role for calpain in the endothelial dysfunction and vascular inflammation of MPO. The MPO/calpain/PP2A signaling pathway may provide novel pharmacological targets for the treatment of inflammatory vascular disorders. MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating endothelial dysfunction. The molecular mechanisms of the endothelial damaging action of MPO remain though largely elusive. Calpain is a calcium-dependent protease expressed in the vascular wall. Activation of calpains has been implicated in inflammatory disorders of the vasculature. Using endothelial cells and genetically modified mice, this study identifies the µ-calpain isoform as novel downstream signaling target of MPO in endothelial dysfunction. Mouse lung microvascular endothelial cells were stimulated with 10 nmol/L MPO for 180 minutes. MPO denitrosylated µ-calpain C-terminus domain, and time dependently activated µ-calpain, but not the m-calpain isoform. MPO also reduced Thr AMPK (AMP-activated protein kinase) and Ser eNOS (endothelial nitric oxide synthase) phosphorylation via upregulation of PP2A (protein phosphatase 2) expression. At the functional level, MPO increased endothelial VCAM-1 (vascular cell adhesion molecule 1) abundance and the adhesion of leukocytes to the mouse aorta. In MPO-treated endothelial cells, pharmacological inhibition of calpain activity attenuated expression of VCAM-1 and PP2A, and restored Thr AMPK and Ser eNOS phosphorylation. Compared with wild-type mice, µ-calpain deficient mice experienced reduced leukocyte adhesion to the aortic endothelium in response to MPO. Our data first establish a role for calpain in the endothelial dysfunction and vascular inflammation of MPO. The MPO/calpain/PP2A signaling pathway may provide novel pharmacological targets for the treatment of inflammatory vascular disorders. |
Author | Scalia, Rosario Preston, Kyle Eguchi, Satoru Etwebi, Zienab Landesberg, Gavin |
AuthorAffiliation | From the Department of Physiology and the Cardiovascular Research Center, Temple University, Philadelphia, PA |
AuthorAffiliation_xml | – name: From the Department of Physiology and the Cardiovascular Research Center, Temple University, Philadelphia, PA |
Author_xml | – sequence: 1 givenname: Zienab surname: Etwebi fullname: Etwebi, Zienab organization: From the Department of Physiology and the Cardiovascular Research Center, Temple University, Philadelphia, PA – sequence: 2 givenname: Gavin surname: Landesberg fullname: Landesberg, Gavin – sequence: 3 givenname: Kyle surname: Preston fullname: Preston, Kyle – sequence: 4 givenname: Satoru surname: Eguchi fullname: Eguchi, Satoru – sequence: 5 givenname: Rosario surname: Scalia fullname: Scalia, Rosario |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29507101$$D View this record in MEDLINE/PubMed |
BookMark | eNqNkE9vEzEQxS1URNPCV0DmVg5bPGt7_xw4RGkgkZomKkWC08przyoLjr1d76qkn75uUzhwQFi2Rn7-vRn5nZAj5x0S8g7YOUAGHxbfN_Prm_nVl-X6arqYRjE_B8aZfEEmIFORCJnxIzJhUIqkBPh2TE5C-MEYCCHyV-Q4LSXLgcGE3K9Qb5Vrw9Bqeu0tUt_QYYt0pqxux11ygR06g26gm94PqMLTU6daR-N-JOfO-Fhtqyy92IdmdHpovaNLZ0aNhtZ7utqs6dlqj9Z32PtfrYlt3r8mLxtlA755rqfk66f5zWyRXK4_L2fTy0SLLJcJoBElL2qtoCyKtFaywFpywDSqSnANtVQouWSGZ4UxmaxlnkOT1Zg2eV3yU3J26Nv1_nbEMFS7Nmi0Vjn0Y6hSBpBmZSlERMsDqnsfQo9N1fXtTvX7Clj1GH31V_RRzKun6KP37fOYsd6h-eP8nXUEPh6AO28H7MNPO95hX21R2WH7XwPEP_wsLpFmRRK_UzARb0k8nPMHqRWnBA |
CitedBy_id | crossref_primary_10_1161_HYPERTENSIONAHA_118_10441 crossref_primary_10_3389_fphar_2022_920977 crossref_primary_10_1038_s41586_019_1688_z crossref_primary_10_1161_HYPERTENSIONAHA_120_15200 crossref_primary_10_3390_antiox11050874 crossref_primary_10_1016_j_bbrc_2019_06_063 crossref_primary_10_1089_vim_2022_0007 crossref_primary_10_1186_s12967_021_03022_x crossref_primary_10_1016_j_ejphar_2022_174940 crossref_primary_10_2478_prolas_2023_0005 crossref_primary_10_1038_s41467_022_34910_5 crossref_primary_10_3389_fcvm_2021_745009 crossref_primary_10_1186_s12885_020_07058_y crossref_primary_10_1016_j_ajpath_2021_06_006 crossref_primary_10_1016_j_pharmthera_2020_107685 crossref_primary_10_3390_antiox13010132 crossref_primary_10_1016_j_lfs_2023_121867 crossref_primary_10_1016_j_jgr_2022_07_006 crossref_primary_10_1016_j_pharmthera_2020_107711 crossref_primary_10_3389_fphys_2020_566410 crossref_primary_10_14814_phy2_15411 crossref_primary_10_1016_j_pharmthera_2020_107715 crossref_primary_10_1161_ATVBAHA_119_312725 crossref_primary_10_1089_ars_2020_8030 crossref_primary_10_1016_j_intimp_2023_110803 crossref_primary_10_1016_j_bbrc_2024_149681 crossref_primary_10_1089_ars_2018_7607 crossref_primary_10_1161_ATVBAHA_120_315452 |
Cites_doi | 10.1161/CIRCULATIONAHA.112.000682 10.1016/S0002-9440(10)64845-6 10.4049/jimmunol.170.1.287 10.1007/s13577-012-0042-7 10.1016/j.jvs.2005.01.013 10.1161/01.RES.76.1.30 10.1016/j.amjmed.2003.10.025 10.1111/j.1742-4658.2008.06394.x 10.1016/j.freeradbiomed.2011.12.001 10.1161/01.CIR.0000140262.20831.8F 10.2337/diabetes.54.4.1132 10.1111/j.1432-1033.1995.tb20498.x 10.2337/diabetes.53.11.2950 10.1152/physrev.00029.2002 10.1161/01.ATV.0000250932.24151.50 10.1152/ajpcell.2000.279.3.C806 10.1073/pnas.2435008100 10.1038/sj.emboj.7600110 10.1161/HYPERTENSIONAHA.116.08854 10.1111/eci.12564 10.1186/s40478-017-0431-y 10.1126/science.1106830 10.1016/j.redox.2017.02.022 10.1016/j.biochi.2010.03.020 10.1016/j.bbrc.2017.01.132 10.1152/ajpendo.00510.2005 10.1111/j.1432-1033.1989.tb15186.x 10.1074/jbc.M211926200 10.1111/j.1600-6143.2005.01077.x 10.2337/db14-0784 10.1182/blood-2010-05-284513 10.1111/j.1742-4658.2007.06133.x 10.1016/j.cmet.2010.03.013 10.1186/s13104-015-1677-8 10.1038/21218 10.4049/jimmunol.163.6.3441 10.1001/jama.286.17.2136 10.1177/1933719114557899 10.1080/13510002.2016.1256119 10.1371/journal.pone.0151960 10.1084/jem.20041315 10.1016/S0014-5793(98)01705-0 10.1083/jcb.200206089 10.1002/1873-3468.12617 10.1172/JCI118074 10.1161/CIRCRESAHA.110.229393 10.1074/jbc.M608310200 10.1006/bbrc.1995.1285 10.1002/(SICI)1097-4644(19970801)66:2<197::AID-JCB7>3.0.CO;2-L 10.1097/01.shk.0000095056.62263.b2 10.1172/JCI118018 10.1016/j.freeradbiomed.2008.09.034 10.1093/aje/154.8.758 10.4049/jimmunol.1300972 10.1074/jbc.275.9.6123 10.1152/ajplung.2000.278.6.L1204 10.1096/fj.99-0645com 10.1038/33934 10.1016/j.foodchem.2016.06.104 10.1016/j.niox.2005.04.002 10.1182/blood-2003-08-2974 10.1096/fj.02-1213fje 10.1016/j.tem.2012.10.008 10.1074/jbc.M212831200 10.1016/j.freeradbiomed.2004.06.003 10.1074/jbc.M803638200 |
ContentType | Journal Article |
Copyright | 2018 American Heart Association, Inc 2018 American Heart Association, Inc. |
Copyright_xml | – notice: 2018 American Heart Association, Inc – notice: 2018 American Heart Association, Inc. |
DBID | CGR CUY CVF ECM EIF NPM AAYXX CITATION 7X8 |
DOI | 10.1161/HYPERTENSIONAHA.117.10305 |
DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef MEDLINE - Academic |
DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef MEDLINE - Academic |
DatabaseTitleList | MEDLINE - Academic CrossRef MEDLINE |
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 | Medicine |
EISSN | 1524-4563 |
EndPage | 770 |
ExternalDocumentID | 10_1161_HYPERTENSIONAHA_117_10305 29507101 10.1161/HYPERTENSIONAHA.117.10305 00004268-201804000-00033 |
Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
GrantInformation_xml | – fundername: NHLBI NIH HHS grantid: R01 HL133248 – fundername: NIDDK NIH HHS grantid: R01 DK064344 – fundername: NHLBI NIH HHS grantid: R01 HL128324 – fundername: NIDDK NIH HHS grantid: R01 DK111042 – fundername: NIDDK NIH HHS grantid: R01 DK096521 |
GroupedDBID | - .XZ .Z2 01R 08R 0R 1J1 2WC 3O- 40H 4Q1 4Q2 4Q3 53G 55 5GY 5RE 5VS 71W 77Y 7O 7O~ AAAXR AAMOA AAMTA AAPBV AARTV AAXQO AAYEP ABBUW ABFLS ABOCM ABXVJ ABZAD ACDDN ACEWG ACGFS ACWDW ACWRI ACXNZ ADBBV ADFPA ADNKB AE3 AENEX AFFNX AFUWQ AHMBA AHULI AHVBC AIJEX AJIOK AJNYG AJYGW ALMA_UNASSIGNED_HOLDINGS AMJPA ASCII AWKKM BAWUL BOYCO BQLVK C1A C45 CS3 DIK DUNZO E.X E3Z EBS EJD EX3 F2K F2L F2M F2N F5P FL- FW0 GJ GX1 H0 H0~ H13 HZ IKYAY IN IN~ JF9 JG8 JK3 JK8 K8S KD2 KMI KQ8 L-C L7B LI0 N9A N~7 N~B N~M O0- O9- OAG OAH OB3 OCUKA ODA OGROG OHASI OK1 OL1 OLG OLH OLU OLV OLW OLY OLZ OPUJH ORVUJ OUVQU OVD OVDNE OVIDH OVLEI OWW OWY OXXIT P-K P2P PQEST PQQKQ R58 RAH RHF RIG RLZ RSW S4R S4S V2I WH7 WOQ WOW X3V X3W X7M XZ YHZ Z2 ZA5 ZGI --- .-D .3C .55 .GJ 0R~ 18M AAAAV AAFWJ AAGIX AAHPQ AAIQE AAJCS AAQKA AASCR AASOK ABASU ABDIG ABJNI ABQRW ABVCZ ACCJW ACGFO ACILI ACLDA ACXJB ADGGA ADHPY AE6 AEBDS AEETU AFDTB AFEXH AGINI AHOMT AHQNM AHRYX AINUH AJNWD AJZMW AKULP ALMTX AMKUR AMNEI AOHHW BCGUY BS7 CGR CUY CVF DIWNM ECM EEVPB EIF ERAAH FCALG GNXGY GQDEL HLJTE HZ~ IKREB IPNFZ K-A K-F N4W NPM ODMTH OHYEH OWBYB OWU OWV OWX OWZ T8P TEORI TR2 TSPGW VVN W3M W8F XXN XYM YFH YOC YYM YYP ZFV ZZMQN AAYXX CITATION 7X8 |
ID | FETCH-LOGICAL-c4675-1ed4938bca19882ba58eb531e2938a43c1b5ae5350d368dd65b5771f6be2f7b93 |
ISSN | 0194-911X |
IngestDate | Fri Aug 16 08:44:06 EDT 2024 Fri Aug 23 00:39:07 EDT 2024 Wed Oct 16 00:50:53 EDT 2024 Thu Aug 13 19:44:27 EDT 2020 Thu Aug 13 19:52:28 EDT 2020 |
IsDoiOpenAccess | false |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 4 |
Keywords | calpain cell adhesion molecules endothelial cells inflammation peroxidase |
Language | English |
License | 2018 American Heart Association, Inc. |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c4675-1ed4938bca19882ba58eb531e2938a43c1b5ae5350d368dd65b5771f6be2f7b93 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
OpenAccessLink | https://www.ahajournals.org/doi/pdf/10.1161/HYPERTENSIONAHA.117.10305 |
PMID | 29507101 |
PQID | 2011269944 |
PQPubID | 23479 |
PageCount | 10 |
ParticipantIDs | proquest_miscellaneous_2011269944 crossref_primary_10_1161_HYPERTENSIONAHA_117_10305 pubmed_primary_29507101 wolterskluwer_health_10_1161_HYPERTENSIONAHA_117_10305 wolterskluwer_health_00004268-201804000-00033 |
ProviderPackageCode | L-C C45 7O~ AARTV ADFPA OLH ASCII OLG AAMOA ODA ABZAD ABBUW JK3 ADNKB JK8 H0~ 1J1 OLV OLU JG8 OLW OLZ OLY F2K F2M F2L F2N OHASI AHVBC AJNYG FL- KMI K8S OGROG OVLEI AJIOK OPUJH V2I .XZ S4R S4S 4Q1 DUNZO OAG 4Q2 OVDNE 4Q3 AMJPA OAH OVD 71W AHULI ACEWG OB3 .Z2 N~7 IKYAY OVIDH AWKKM 40H N~B OUVQU ORVUJ X3V X3W ACDDN ACWRI BOYCO AIJEX AAXQO AAMTA AAAXR E.X OWW OCUKA OWY 01R ACXNZ OL1 ABXVJ IN~ KD2 OXXIT 77Y ACWDW JF9 FW0 |
PublicationCentury | 2000 |
PublicationDate | 2018-April |
PublicationDateYYYYMMDD | 2018-04-01 |
PublicationDate_xml | – month: 04 year: 2018 text: 2018-April |
PublicationDecade | 2010 |
PublicationPlace | United States |
PublicationPlace_xml | – name: United States |
PublicationTitle | Hypertension (Dallas, Tex. 1979) |
PublicationTitleAlternate | Hypertension |
PublicationYear | 2018 |
Publisher | American Heart Association, Inc |
Publisher_xml | – name: American Heart Association, Inc |
References | 29507102 - Hypertension. 2018 Apr;71(4):574-576 e_1_3_3_50_2 e_1_3_3_16_2 e_1_3_3_18_2 e_1_3_3_39_2 e_1_3_3_12_2 e_1_3_3_37_2 e_1_3_3_58_2 e_1_3_3_14_2 e_1_3_3_35_2 e_1_3_3_56_2 e_1_3_3_33_2 e_1_3_3_54_2 e_1_3_3_10_2 e_1_3_3_31_2 e_1_3_3_52_2 e_1_3_3_40_2 e_1_3_3_61_2 e_1_3_3_5_2 e_1_3_3_7_2 e_1_3_3_9_2 e_1_3_3_27_2 e_1_3_3_29_2 e_1_3_3_23_2 e_1_3_3_48_2 e_1_3_3_25_2 e_1_3_3_46_2 e_1_3_3_67_2 e_1_3_3_44_2 e_1_3_3_65_2 e_1_3_3_3_2 e_1_3_3_21_2 e_1_3_3_42_2 e_1_3_3_63_2 Cunha FQ (e_1_3_3_51_2) 1994; 81 e_1_3_3_17_2 e_1_3_3_19_2 e_1_3_3_38_2 e_1_3_3_13_2 e_1_3_3_36_2 e_1_3_3_59_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_57_2 e_1_3_3_32_2 e_1_3_3_55_2 e_1_3_3_11_2 e_1_3_3_30_2 e_1_3_3_53_2 e_1_3_3_62_2 e_1_3_3_60_2 e_1_3_3_6_2 e_1_3_3_8_2 e_1_3_3_28_2 e_1_3_3_49_2 e_1_3_3_24_2 e_1_3_3_47_2 e_1_3_3_26_2 e_1_3_3_45_2 e_1_3_3_68_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_43_2 e_1_3_3_66_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_41_2 e_1_3_3_64_2 |
References_xml | – ident: e_1_3_3_3_2 doi: 10.1161/CIRCULATIONAHA.112.000682 – ident: e_1_3_3_37_2 doi: 10.1016/S0002-9440(10)64845-6 – ident: e_1_3_3_47_2 doi: 10.4049/jimmunol.170.1.287 – ident: e_1_3_3_63_2 doi: 10.1007/s13577-012-0042-7 – ident: e_1_3_3_4_2 doi: 10.1016/j.jvs.2005.01.013 – ident: e_1_3_3_60_2 doi: 10.1161/01.RES.76.1.30 – ident: e_1_3_3_11_2 doi: 10.1016/j.amjmed.2003.10.025 – ident: e_1_3_3_53_2 doi: 10.1111/j.1742-4658.2008.06394.x – ident: e_1_3_3_54_2 doi: 10.1016/j.freeradbiomed.2011.12.001 – ident: e_1_3_3_6_2 doi: 10.1161/01.CIR.0000140262.20831.8F – ident: e_1_3_3_18_2 doi: 10.2337/diabetes.54.4.1132 – ident: e_1_3_3_42_2 doi: 10.1111/j.1432-1033.1995.tb20498.x – ident: e_1_3_3_43_2 doi: 10.2337/diabetes.53.11.2950 – ident: e_1_3_3_12_2 doi: 10.1152/physrev.00029.2002 – ident: e_1_3_3_35_2 doi: 10.1161/01.ATV.0000250932.24151.50 – ident: e_1_3_3_48_2 doi: 10.1152/ajpcell.2000.279.3.C806 – ident: e_1_3_3_49_2 doi: 10.1073/pnas.2435008100 – ident: e_1_3_3_28_2 doi: 10.1038/sj.emboj.7600110 – ident: e_1_3_3_7_2 doi: 10.1161/HYPERTENSIONAHA.116.08854 – ident: e_1_3_3_44_2 doi: 10.1111/eci.12564 – ident: e_1_3_3_55_2 doi: 10.1186/s40478-017-0431-y – ident: e_1_3_3_33_2 doi: 10.1126/science.1106830 – ident: e_1_3_3_34_2 doi: 10.1016/j.redox.2017.02.022 – ident: e_1_3_3_40_2 doi: 10.1016/j.biochi.2010.03.020 – ident: e_1_3_3_45_2 doi: 10.1016/j.bbrc.2017.01.132 – ident: e_1_3_3_27_2 doi: 10.1152/ajpendo.00510.2005 – ident: e_1_3_3_41_2 doi: 10.1111/j.1432-1033.1989.tb15186.x – ident: e_1_3_3_38_2 doi: 10.1074/jbc.M211926200 – ident: e_1_3_3_68_2 doi: 10.1111/j.1600-6143.2005.01077.x – ident: e_1_3_3_36_2 doi: 10.2337/db14-0784 – ident: e_1_3_3_62_2 doi: 10.1182/blood-2010-05-284513 – ident: e_1_3_3_52_2 doi: 10.1111/j.1742-4658.2007.06133.x – ident: e_1_3_3_19_2 doi: 10.1016/j.cmet.2010.03.013 – ident: e_1_3_3_21_2 doi: 10.1186/s13104-015-1677-8 – ident: e_1_3_3_25_2 doi: 10.1038/21218 – ident: e_1_3_3_32_2 doi: 10.4049/jimmunol.163.6.3441 – ident: e_1_3_3_10_2 doi: 10.1001/jama.286.17.2136 – ident: e_1_3_3_46_2 doi: 10.1177/1933719114557899 – ident: e_1_3_3_8_2 doi: 10.1080/13510002.2016.1256119 – ident: e_1_3_3_61_2 doi: 10.1371/journal.pone.0151960 – ident: e_1_3_3_16_2 doi: 10.1084/jem.20041315 – ident: e_1_3_3_26_2 doi: 10.1016/S0014-5793(98)01705-0 – volume: 81 start-page: 211 year: 1994 ident: e_1_3_3_51_2 article-title: Differential induction of nitric oxide synthase in various organs of the mouse during endotoxaemia: role of TNF-alpha and IL-1-beta. publication-title: Immunology contributor: fullname: Cunha FQ – ident: e_1_3_3_65_2 doi: 10.1083/jcb.200206089 – ident: e_1_3_3_29_2 doi: 10.1002/1873-3468.12617 – ident: e_1_3_3_31_2 doi: 10.1172/JCI118074 – ident: e_1_3_3_67_2 doi: 10.1161/CIRCRESAHA.110.229393 – ident: e_1_3_3_30_2 doi: 10.1074/jbc.M608310200 – ident: e_1_3_3_22_2 doi: 10.1006/bbrc.1995.1285 – ident: e_1_3_3_14_2 doi: 10.1002/(SICI)1097-4644(19970801)66:2<197::AID-JCB7>3.0.CO;2-L – ident: e_1_3_3_64_2 doi: 10.1097/01.shk.0000095056.62263.b2 – ident: e_1_3_3_20_2 doi: 10.1172/JCI118018 – ident: e_1_3_3_24_2 doi: 10.1016/j.freeradbiomed.2008.09.034 – ident: e_1_3_3_5_2 doi: 10.1093/aje/154.8.758 – ident: e_1_3_3_13_2 doi: 10.4049/jimmunol.1300972 – ident: e_1_3_3_56_2 doi: 10.1074/jbc.275.9.6123 – ident: e_1_3_3_57_2 doi: 10.1152/ajplung.2000.278.6.L1204 – ident: e_1_3_3_17_2 doi: 10.1096/fj.99-0645com – ident: e_1_3_3_59_2 doi: 10.1038/33934 – ident: e_1_3_3_23_2 doi: 10.1016/j.foodchem.2016.06.104 – ident: e_1_3_3_50_2 doi: 10.1016/j.niox.2005.04.002 – ident: e_1_3_3_66_2 doi: 10.1182/blood-2003-08-2974 – ident: e_1_3_3_58_2 doi: 10.1096/fj.02-1213fje – ident: e_1_3_3_2_2 doi: 10.1016/j.tem.2012.10.008 – ident: e_1_3_3_39_2 doi: 10.1074/jbc.M212831200 – ident: e_1_3_3_9_2 doi: 10.1016/j.freeradbiomed.2004.06.003 – ident: e_1_3_3_15_2 doi: 10.1074/jbc.M803638200 |
SSID | ssj0014447 |
Score | 2.451012 |
Snippet | MPO (myeloperoxidase) is a peroxidase enzyme secreted by activated leukocytes that plays a pathogenic role in cardiovascular disease, mainly by initiating... |
SourceID | proquest crossref pubmed wolterskluwer |
SourceType | Aggregation Database Index Database Publisher |
StartPage | 761 |
SubjectTerms | Animals Animals, Genetically Modified Aorta - metabolism Aorta - pathology Calpain - metabolism Cell Adhesion - physiology Cell Adhesion Molecules - metabolism Cell Culture Techniques Endothelial Cells - immunology Endothelial Cells - metabolism Inflammation - immunology Leukocytes - physiology Mice Peroxidase - metabolism Protein Phosphatase 2 - metabolism Signal Transduction Up-Regulation Vascular Diseases - immunology Vascular Diseases - metabolism |
Title | Mechanistic Role of the Calcium-Dependent Protease Calpain in the Endothelial Dysfunction Induced by MPO (Myeloperoxidase) |
URI | http://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00004268-201804000-00033 https://www.ncbi.nlm.nih.gov/pubmed/29507101 https://search.proquest.com/docview/2011269944 |
Volume | 71 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1ba9swFBZZB2VjjN2X3VBhDxvFrWX5psfQuA1bk5aRQLYXY9nKCMvikjhb03-xf7xzZMVxm451g2CCI4Tx-XJu-s45hLx1FRhFW3lW5nAOAQoLLZkFNra7A8Sk4HArrHfu9vzOwP0w9IaNxq8aa2lRyL304tq6kv-RKtwDuWKV7D9IttoUbsB3kC9cQcJwvZGMuwrrdnWr5d1PhiaIjuRBMknHi-9W20y4LbAeoMCDGPzpLBlX9MZommEJ1gTz5u3lHK2cBgRO9EhL57R7eoJuaHeJ5CI1y8_HWTKvejkZv7YD4exMk-E1msI25udLBpI639tlIhC1nENUgPLWNIIvoFkSWbGCMKM9XzHOjpIf4wq6SBUxTP-Py0mFxugrDnMpU9tFPlvUkxgAiDX3RRnF67gWOHO8rpnL4SwGgW5NzQY-q1nsoBw9smkMfDQGnc-nEYQGPbRNrU4LT6mx04DtrS3g6tS_dxIfDo6P43407N8it51AeMgSPRpWrCEIP91gm-yY7ff_uPllN2cjdrlL7v3MkQ4x_6arIWo-Tf8BuW-CEdoqkfWQNNT0EdnuGrrFY3JRAxhFgNF8RAEudANgdAUwagBG4YMrawCjNYBRAzAqlxQARt9dgdf7J2RwGPUPOpYZ1mGlYGs9i6nMFTyUacIERG0y8UIlQcEr8CfDxOUpk16iPO7ZGffDLPM96QUBG_lSOaNACv6UbE3zqXpOqMODkQRbI1PFXCVgoWLYF9ERUoF5EU3irN5tfFb2ZIl1LOuz-IpAsJd9rAXSJDsrKcSgQfFYLJmqfDGP0QV2fCFct0meleKptnUExks2axLrkrzisko51iG246NaYiHaQ92mgfMm8a9d_9fHfHGDx3xJ7qz_Q6_IVjFbqNfgGhfyjQbrb1NutmM |
link.rule.ids | 315,786,790,27955,27956 |
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=Mechanistic+Role+of+the+Calcium-Dependent+Protease+Calpain+in+the+Endothelial+Dysfunction+Induced+by+MPO+%28Myeloperoxidase%29&rft.jtitle=Hypertension+%28Dallas%2C+Tex.+1979%29&rft.au=Etwebi%2C+Zienab&rft.au=Landesberg%2C+Gavin&rft.au=Preston%2C+Kyle&rft.au=Eguchi%2C+Satoru&rft.date=2018-04-01&rft.eissn=1524-4563&rft.volume=71&rft.issue=4&rft.spage=761&rft.epage=770&rft_id=info:doi/10.1161%2FHYPERTENSIONAHA.117.10305&rft.externalDBID=NO_FULL_TEXT |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0194-911X&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0194-911X&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0194-911X&client=summon |