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Article: Genomic changes in regenerated porcine coronary arterial endothelial cells
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TitleGenomic changes in regenerated porcine coronary arterial endothelial cells
 
AuthorsLee, MYK1
Tse, HF1
Siu, CW1
Zhu, SG1
Man, RYK1
Vanhoutte, PM1
 
KeywordsCoagulation
Endothelial regeneration
Extracellular matrix
Genomics
Lipids
Nitric oxide
ROS
 
Issue Date2007
 
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642
 
CitationArteriosclerosis, Thrombosis, And Vascular Biology, 2007, v. 27 n. 11, p. 2443-2449 [How to Cite?]
DOI: http://dx.doi.org/10.1161/ATVBAHA.107.141705
 
AbstractOBJECTIVE - Genomic changes were defined in cultures of regenerated porcine coronary endothelial cells to explain the alterations that underlie their dysfunction. METHODS AND RESULTS - Regeneration of the endothelium was triggered in vivo by endothelial balloon denudation. After 28 days, both left circumflex (native cells) and left anterior descending (regenerated cells) coronary arteries were dissected, their endothelial cells harvested, and primary cultures established. The basal cyclic GMP production was reduced in regenerated cells without significant reduction in the response to bradykinin and A23187. The mRNA expression levels in both native and regenerated cells were measured by microarray and RT-PCR. The comparison revealed genomic changes related to vasomotor control (cyclooxygenase-1, angiotensin II receptor), coagulation (F2 and TFPI), oxidative stress (Mn SOD, GPX3, and GSR), lipid metabolism (PLA2 and HPGD), and extracellular matrix (MMPs). A-FABP and MMP7 were induced by regeneration. RT-PCR revealed upregulation of A-FABP and downregulation of eNOS and TR. The differential gene expression profiles were confirmed at the protein level by Western blotting for eNOS, F2, Mn SOD, MMP7, and TR. CONCLUSIONS - Cultures from regenerated coronary endothelial cells exhibit genomic changes explaining endothelial dysfunction and suggesting facilitation of coagulation, lipid peroxidation, and extracellular matrix remodeling. © 2007 American Heart Association, Inc.
 
ISSN1079-5642
2012 Impact Factor: 6.338
2012 SCImago Journal Rankings: 2.609
 
DOIhttp://dx.doi.org/10.1161/ATVBAHA.107.141705
 
ISI Accession Number IDWOS:000250424700025
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLee, MYK
 
dc.contributor.authorTse, HF
 
dc.contributor.authorSiu, CW
 
dc.contributor.authorZhu, SG
 
dc.contributor.authorMan, RYK
 
dc.contributor.authorVanhoutte, PM
 
dc.date.accessioned2010-09-06T07:23:55Z
 
dc.date.available2010-09-06T07:23:55Z
 
dc.date.issued2007
 
dc.description.abstractOBJECTIVE - Genomic changes were defined in cultures of regenerated porcine coronary endothelial cells to explain the alterations that underlie their dysfunction. METHODS AND RESULTS - Regeneration of the endothelium was triggered in vivo by endothelial balloon denudation. After 28 days, both left circumflex (native cells) and left anterior descending (regenerated cells) coronary arteries were dissected, their endothelial cells harvested, and primary cultures established. The basal cyclic GMP production was reduced in regenerated cells without significant reduction in the response to bradykinin and A23187. The mRNA expression levels in both native and regenerated cells were measured by microarray and RT-PCR. The comparison revealed genomic changes related to vasomotor control (cyclooxygenase-1, angiotensin II receptor), coagulation (F2 and TFPI), oxidative stress (Mn SOD, GPX3, and GSR), lipid metabolism (PLA2 and HPGD), and extracellular matrix (MMPs). A-FABP and MMP7 were induced by regeneration. RT-PCR revealed upregulation of A-FABP and downregulation of eNOS and TR. The differential gene expression profiles were confirmed at the protein level by Western blotting for eNOS, F2, Mn SOD, MMP7, and TR. CONCLUSIONS - Cultures from regenerated coronary endothelial cells exhibit genomic changes explaining endothelial dysfunction and suggesting facilitation of coagulation, lipid peroxidation, and extracellular matrix remodeling. © 2007 American Heart Association, Inc.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationArteriosclerosis, Thrombosis, And Vascular Biology, 2007, v. 27 n. 11, p. 2443-2449 [How to Cite?]
DOI: http://dx.doi.org/10.1161/ATVBAHA.107.141705
 
dc.identifier.doihttp://dx.doi.org/10.1161/ATVBAHA.107.141705
 
dc.identifier.epage2449
 
dc.identifier.hkuros147765
 
dc.identifier.isiWOS:000250424700025
 
dc.identifier.issn1079-5642
2012 Impact Factor: 6.338
2012 SCImago Journal Rankings: 2.609
 
dc.identifier.issue11
 
dc.identifier.openurl
 
dc.identifier.scopuseid_2-s2.0-36048970965
 
dc.identifier.spage2443
 
dc.identifier.urihttp://hdl.handle.net/10722/76692
 
dc.identifier.volume27
 
dc.languageeng
 
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642
 
dc.publisher.placeUnited States
 
dc.relation.ispartofArteriosclerosis, Thrombosis, and Vascular Biology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsArteriosclerosis, Thrombosis, and Vascular Biology. Copyright © Lippincott Williams & Wilkins.
 
dc.subjectCoagulation
 
dc.subjectEndothelial regeneration
 
dc.subjectExtracellular matrix
 
dc.subjectGenomics
 
dc.subjectLipids
 
dc.subjectNitric oxide
 
dc.subjectROS
 
dc.titleGenomic changes in regenerated porcine coronary arterial endothelial cells
 
dc.typeArticle
 
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<subject>Coagulation</subject>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine