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- Publisher Website: 10.1152/physiolgenomics.00136.2007
- Scopus: eid_2-s2.0-40149085142
- PMID: 18056786
- WOS: WOS:000256816300014
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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
Title | Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension |
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Authors | |
Keywords | Endothelium-dependent contractions Endothelium-derived contracting factors Prostacyclin Prostacyclin synthase Real-time quantitative polymerase chain reaction |
Issue Date | 2008 |
Publisher | American Physiological Society |
Citation | Physiological Genomics, 2008, v. 32 n. 3, p. 409-418 How to Cite? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/91747 |
ISSN | 2023 Impact Factor: 2.5 2023 SCImago Journal Rankings: 0.999 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Tang, EHC | en_HK |
dc.contributor.author | Vanhoutte, PM | en_HK |
dc.date.accessioned | 2010-09-17T10:25:21Z | - |
dc.date.available | 2010-09-17T10:25:21Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Physiological Genomics, 2008, v. 32 n. 3, p. 409-418 | en_HK |
dc.identifier.issn | 1094-8341 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/91747 | - |
dc.description.abstract | The 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.language | eng | en_HK |
dc.publisher | American Physiological Society | en_HK |
dc.relation.ispartof | Physiological Genomics | en_HK |
dc.subject | Endothelium-dependent contractions | en_HK |
dc.subject | Endothelium-derived contracting factors | en_HK |
dc.subject | Prostacyclin | en_HK |
dc.subject | Prostacyclin synthase | en_HK |
dc.subject | Real-time quantitative polymerase chain reaction | en_HK |
dc.title | Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Tang, EHC: evatang1@hku.hk | en_HK |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_HK |
dc.identifier.authority | Tang, EHC=rp01382 | en_HK |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1152/physiolgenomics.00136.2007 | en_HK |
dc.identifier.pmid | 18056786 | - |
dc.identifier.scopus | eid_2-s2.0-40149085142 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-40149085142&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 32 | en_HK |
dc.identifier.issue | 3 | en_HK |
dc.identifier.spage | 409 | en_HK |
dc.identifier.epage | 418 | en_HK |
dc.identifier.eissn | 1531-2267 | - |
dc.identifier.isi | WOS:000256816300014 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Tang, EHC=9536518500 | en_HK |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_HK |
dc.identifier.issnl | 1094-8341 | - |