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Article: Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension

TitleGene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension
Authors
KeywordsEndothelium-dependent contractions
Endothelium-derived contracting factors
Prostacyclin
Prostacyclin synthase
Real-time quantitative polymerase chain reaction
Issue Date2008
PublisherAmerican Physiological Society
Citation
Physiological Genomics, 2008, v. 32 n. 3, p. 409-418 How to Cite?
AbstractThe present study was designed to assess whether or not changes in genomic expression of cyclooxygenases (COX-1, COX-2), endothelial nitric oxide synthase (eNOS), and prostanoid synthases in the endothelium and of prostanoid receptors in vascular smooth muscle contribute to the occurrence of endothelium-dependent contractions during aging and hypertension. Gene expression was quantified by real-time PCR using isolated endothelial cells and smooth muscle cells (SMC) from the aorta of Wistar-Kyoto and spontaneously hypertensive rats. Genes for all known prostanoid synthases and receptors were present in endothelial cells and SMC, respectively. Aging caused overexpression of eNOS, COX-1, COX-2, thromboxane synthase, hematopoietic-type prostaglandin D synthase, membrane prostaglandin E synthase-2, and prostaglandin F synthase in endothelial cells and COX-1 and prostaglandin E2 (EP)4 receptors in SMC. Hypertension augmented the expression of COX-1, prostacyclin synthase, thromboxane synthase, and hematopoietic-type prostaglandin D synthase in endothelial cells and prostaglandin D2 (DP), EP3, and EP4 receptors in SMC. The increase in genomic expression of endothelial COX-1 explains why in aging and hypertension the endothelium has greater propensity to release cyclooxygenase-derived vasoconstrictive prostanoids. The expression of prostacyclin synthase was by far the most abundant, explaining why the majority of the COX-1-derived endoperoxides are transformed into prostacyclin, substantiating the role of prostacyclin as an endothelium-derived contracting factor. The expression of thromboxane synthase was increased in the cells of aging or hypertensive rats, explaining why the prostanoid can contribute to endothelium-dependent contractions. It is uncertain whether the gene modifications caused by aging and hypertension directly contribute to endothelium-dependent contractions or rather to vascular aging and the vascular complications of the hypertensive process. Copyright © 2008 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/91747
ISSN
2015 Impact Factor: 2.615
2015 SCImago Journal Rankings: 1.545
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-17T10:25:21Z-
dc.date.available2010-09-17T10:25:21Z-
dc.date.issued2008en_HK
dc.identifier.citationPhysiological Genomics, 2008, v. 32 n. 3, p. 409-418en_HK
dc.identifier.issn1094-8341en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91747-
dc.description.abstractThe present study was designed to assess whether or not changes in genomic expression of cyclooxygenases (COX-1, COX-2), endothelial nitric oxide synthase (eNOS), and prostanoid synthases in the endothelium and of prostanoid receptors in vascular smooth muscle contribute to the occurrence of endothelium-dependent contractions during aging and hypertension. Gene expression was quantified by real-time PCR using isolated endothelial cells and smooth muscle cells (SMC) from the aorta of Wistar-Kyoto and spontaneously hypertensive rats. Genes for all known prostanoid synthases and receptors were present in endothelial cells and SMC, respectively. Aging caused overexpression of eNOS, COX-1, COX-2, thromboxane synthase, hematopoietic-type prostaglandin D synthase, membrane prostaglandin E synthase-2, and prostaglandin F synthase in endothelial cells and COX-1 and prostaglandin E2 (EP)4 receptors in SMC. Hypertension augmented the expression of COX-1, prostacyclin synthase, thromboxane synthase, and hematopoietic-type prostaglandin D synthase in endothelial cells and prostaglandin D2 (DP), EP3, and EP4 receptors in SMC. The increase in genomic expression of endothelial COX-1 explains why in aging and hypertension the endothelium has greater propensity to release cyclooxygenase-derived vasoconstrictive prostanoids. The expression of prostacyclin synthase was by far the most abundant, explaining why the majority of the COX-1-derived endoperoxides are transformed into prostacyclin, substantiating the role of prostacyclin as an endothelium-derived contracting factor. The expression of thromboxane synthase was increased in the cells of aging or hypertensive rats, explaining why the prostanoid can contribute to endothelium-dependent contractions. It is uncertain whether the gene modifications caused by aging and hypertension directly contribute to endothelium-dependent contractions or rather to vascular aging and the vascular complications of the hypertensive process. Copyright © 2008 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Societyen_HK
dc.relation.ispartofPhysiological Genomicsen_HK
dc.subjectEndothelium-dependent contractionsen_HK
dc.subjectEndothelium-derived contracting factorsen_HK
dc.subjectProstacyclinen_HK
dc.subjectProstacyclin synthaseen_HK
dc.subjectReal-time quantitative polymerase chain reactionen_HK
dc.titleGene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertensionen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/physiolgenomics.00136.2007en_HK
dc.identifier.pmid18056786-
dc.identifier.scopuseid_2-s2.0-40149085142en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-40149085142&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume32en_HK
dc.identifier.issue3en_HK
dc.identifier.spage409en_HK
dc.identifier.epage418en_HK
dc.identifier.eissn1531-2267-
dc.identifier.isiWOS:000256816300014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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