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Article: Differential genomic changes caused by cholesterol-and PUFA-rich diets in regenerated porcine coronary endothelial cells

TitleDifferential genomic changes caused by cholesterol-and PUFA-rich diets in regenerated porcine coronary endothelial cells
Authors
KeywordsEndothelium
Fish oil
Microarray
Polyunsaturated fatty acids
Porcine coronary artery angioplasty
Regeneration
Issue Date2012
PublisherAmerican Physiological Society. The Journal's web site is located at http://physiolgenomics.physiology.org/
Citation
Physiological Genomics, 2012, v. 44 n. 10, p. 551-561 How to Cite?
AbstractEndothelial regeneration and dyslipidemia impair endothelium-dependent relaxation, while supplementation with fish oil (FO) prevents it. The genomic impact of different diets was compared in primary cultures derived from native and regenerated endothelial cells. Pigs were fed with high-cholesterol (CHL) or FO-rich diet. Partial in vivo removal of endothelium was performed to induce endothelial regeneration. Native and regenerated cells were harvested, cultured, and prepared for genomic (microarray experiments, real-time PCR) and proteomic (Western blotting) analysis. The analysis identified genomic changes induced by chronic CHL diet in native cultures resembling those induced by in vivo regeneration, as well as those that could be prevented by FO diet. At the protein level, the reduced and increased presences of endothelial nitric oxide synthase and F2, respectively, observed after regeneration combined with CHL diet were alleviated by FO. The comparison of the differential changes induced by regeneration in vivo in endothelial cells from both diet groups revealed a limited number of genes as the most likely contributors to reduction in endothelium-dependent relaxations in porcine coronary arteries lined with regenerated endothelium. © 2012 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/149118
ISSN
2023 Impact Factor: 2.5
2023 SCImago Journal Rankings: 0.999
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
Research Grant Council of Hong KongHKU 780410M
Research Centre of Heart, Brain, Hormone & Healthy Aging of the University of Hong Kong
Les Laboratoires Servier [Neuilly-sur-Seine, France]
Funding Information:

This work was supported by grants from the University of Hong Kong; the Research Grant Council of Hong Kong (HKU 780410M); and the Research Centre of Heart, Brain, Hormone & Healthy Aging of the University of Hong Kong. This study was also supported by an unconditional grant from Les Laboratoires Servier [Neuilly-sur-Seine, France].

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLee, MYKen_HK
dc.contributor.authorCai, Yen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorLiao, SYen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorBai, Ben_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2012-06-22T06:24:15Z-
dc.date.available2012-06-22T06:24:15Z-
dc.date.issued2012en_HK
dc.identifier.citationPhysiological Genomics, 2012, v. 44 n. 10, p. 551-561en_HK
dc.identifier.issn1094-8341en_HK
dc.identifier.urihttp://hdl.handle.net/10722/149118-
dc.description.abstractEndothelial regeneration and dyslipidemia impair endothelium-dependent relaxation, while supplementation with fish oil (FO) prevents it. The genomic impact of different diets was compared in primary cultures derived from native and regenerated endothelial cells. Pigs were fed with high-cholesterol (CHL) or FO-rich diet. Partial in vivo removal of endothelium was performed to induce endothelial regeneration. Native and regenerated cells were harvested, cultured, and prepared for genomic (microarray experiments, real-time PCR) and proteomic (Western blotting) analysis. The analysis identified genomic changes induced by chronic CHL diet in native cultures resembling those induced by in vivo regeneration, as well as those that could be prevented by FO diet. At the protein level, the reduced and increased presences of endothelial nitric oxide synthase and F2, respectively, observed after regeneration combined with CHL diet were alleviated by FO. The comparison of the differential changes induced by regeneration in vivo in endothelial cells from both diet groups revealed a limited number of genes as the most likely contributors to reduction in endothelium-dependent relaxations in porcine coronary arteries lined with regenerated endothelium. © 2012 the American Physiological Society.en_HK
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://physiolgenomics.physiology.org/-
dc.relation.ispartofPhysiological Genomicsen_HK
dc.rightsPhysiological Genomics. Copyright © American Physiological Society-
dc.subjectEndotheliumen_HK
dc.subjectFish oilen_HK
dc.subjectMicroarrayen_HK
dc.subjectPolyunsaturated fatty acidsen_HK
dc.subjectPorcine coronary artery angioplastyen_HK
dc.subjectRegenerationen_HK
dc.titleDifferential genomic changes caused by cholesterol-and PUFA-rich diets in regenerated porcine coronary endothelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailTse, HF: hftse@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/physiolgenomics.00140.2011en_HK
dc.identifier.pmid22454453-
dc.identifier.scopuseid_2-s2.0-84862099772en_HK
dc.identifier.hkuros199999en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84862099772&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume44en_HK
dc.identifier.issue10en_HK
dc.identifier.spage551en_HK
dc.identifier.epage561en_HK
dc.identifier.isiWOS:000304367600002-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectProtective effect of lipocalin-2 deficiency on aging- and dietary obesity-induced endothelial dysfunction-
dc.identifier.scopusauthoridLee, MYK=22980015700en_HK
dc.identifier.scopusauthoridCai, Y=55247545000en_HK
dc.identifier.scopusauthoridWang, Y=54953511800en_HK
dc.identifier.scopusauthoridLiao, SY=22433820700en_HK
dc.identifier.scopusauthoridLiu, Y=54936707200en_HK
dc.identifier.scopusauthoridZhang, Y=35785466900en_HK
dc.identifier.scopusauthoridBai, B=55247646000en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.issnl1094-8341-

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