Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension
Department of Pharmacology, University of Hong Kong, Hong Kong 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...
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| Veröffentlicht in: | Physiological genomics 2008-02, Vol.32 (3), p.409-418 |
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| creator | Tang, Eva H. C Vanhoutte, Paul M |
| description | Department of Pharmacology, University of Hong Kong, Hong Kong
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 E 2 (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 D 2 (DP), EP 3 , and EP 4 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.
endothelium-dependent contractions; endothelium-derived contracting factors; prostacyclin synthase; prostacyclin; real-time quantitative polymerase chain reaction |
| doi_str_mv | 10.1152/physiolgenomics.00136.2007 |
| format | Article |
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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 E 2 (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 D 2 (DP), EP 3 , and EP 4 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.
endothelium-dependent contractions; endothelium-derived contracting factors; prostacyclin synthase; prostacyclin; real-time quantitative polymerase chain reaction</description><identifier>ISSN: 1094-8341</identifier><identifier>EISSN: 1531-2267</identifier><identifier>DOI: 10.1152/physiolgenomics.00136.2007</identifier><identifier>PMID: 18056786</identifier><language>eng</language><publisher>United States: Am Physiological Soc</publisher><subject>Acetylcholine - pharmacology ; Aging - genetics ; Animals ; Aorta, Thoracic - drug effects ; Cyclooxygenase 1 - biosynthesis ; Cyclooxygenase 1 - genetics ; Endothelial Cells - metabolism ; Enzyme Induction ; Gene Expression Profiling ; Gene Expression Regulation ; Hypertension - genetics ; Membrane Proteins - biosynthesis ; Membrane Proteins - genetics ; Muscle Proteins - biosynthesis ; Muscle Proteins - genetics ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - metabolism ; Nitric Oxide Synthase Type II - biosynthesis ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type III ; Phenylephrine - pharmacology ; Prostaglandin-Endoperoxide Synthases - biosynthesis ; Prostaglandin-Endoperoxide Synthases - genetics ; Prostaglandins - biosynthesis ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptors, Prostaglandin - biosynthesis ; Receptors, Prostaglandin - genetics</subject><ispartof>Physiological genomics, 2008-02, Vol.32 (3), p.409-418</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-b2e33ddc692962bec78628f6b1366178fe49c5f0a28c143a1beaaf80ad9a0bc23</citedby><cites>FETCH-LOGICAL-c483t-b2e33ddc692962bec78628f6b1366178fe49c5f0a28c143a1beaaf80ad9a0bc23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18056786$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Eva H. C</creatorcontrib><creatorcontrib>Vanhoutte, Paul M</creatorcontrib><title>Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension</title><title>Physiological genomics</title><addtitle>Physiol Genomics</addtitle><description>Department of Pharmacology, University of Hong Kong, Hong Kong
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 E 2 (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 D 2 (DP), EP 3 , and EP 4 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.
endothelium-dependent contractions; endothelium-derived contracting factors; prostacyclin synthase; prostacyclin; real-time quantitative polymerase chain reaction</description><subject>Acetylcholine - pharmacology</subject><subject>Aging - genetics</subject><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Cyclooxygenase 1 - biosynthesis</subject><subject>Cyclooxygenase 1 - genetics</subject><subject>Endothelial Cells - metabolism</subject><subject>Enzyme Induction</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Hypertension - genetics</subject><subject>Membrane Proteins - biosynthesis</subject><subject>Membrane Proteins - genetics</subject><subject>Muscle Proteins - biosynthesis</subject><subject>Muscle Proteins - genetics</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Nitric Oxide Synthase Type II - biosynthesis</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Phenylephrine - pharmacology</subject><subject>Prostaglandin-Endoperoxide Synthases - biosynthesis</subject><subject>Prostaglandin-Endoperoxide Synthases - genetics</subject><subject>Prostaglandins - biosynthesis</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Receptors, Prostaglandin - biosynthesis</subject><subject>Receptors, Prostaglandin - genetics</subject><issn>1094-8341</issn><issn>1531-2267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctu1TAURS0EoqXwC8hiwCwXP_JkglBFC1IlJmVsOc5JYuTYwSeB5mf4VnwfFehKjGxZa--zjzchbzjbcV6Id_O4oQ1uAB8ma3DHGJflTjBWPSGXvJA8E6KsnqY7a_Ksljm_IC8Qvycur-riObngNSvKqi4vye9b8EDhYY6AydRTM2o_ANLQ0zkGXLQPtqO4-WXUmN6tp-C7sIzgrHbUgHNIte_-pSMYmJcQD_RPjWZ1OlKcQpLRaUXj4CQ0ekXoaLtRPVg_HIzGbYa4gN_HeUme9dohvDqdV-Tbzaf768_Z3dfbL9cf7zKT13LJWgFSdp0pG9GUogWTdhN1X7bpY0pe1T3kjSl6pkVteC41b0Hrvma6azRrjZBX5O3RN23xYwVc1GRxH1F7CCuqikleybJI4PsjaNK6GKFXc7STjpviTO3bUWftqEM7at9OEr8-TVnbCbq_0lMdCfhwBEY7jL9shEe3MGzqZnXuHh6W8wlSKKly1qi565OD_L_DebRHpfwDuybBpA</recordid><startdate>20080219</startdate><enddate>20080219</enddate><creator>Tang, Eva H. C</creator><creator>Vanhoutte, Paul M</creator><general>Am Physiological Soc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20080219</creationdate><title>Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension</title><author>Tang, Eva H. C ; Vanhoutte, Paul M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-b2e33ddc692962bec78628f6b1366178fe49c5f0a28c143a1beaaf80ad9a0bc23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Aging - genetics</topic><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Cyclooxygenase 1 - biosynthesis</topic><topic>Cyclooxygenase 1 - genetics</topic><topic>Endothelial Cells - metabolism</topic><topic>Enzyme Induction</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Hypertension - genetics</topic><topic>Membrane Proteins - biosynthesis</topic><topic>Membrane Proteins - genetics</topic><topic>Muscle Proteins - biosynthesis</topic><topic>Muscle Proteins - genetics</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Nitric Oxide Synthase Type II - biosynthesis</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Phenylephrine - pharmacology</topic><topic>Prostaglandin-Endoperoxide Synthases - biosynthesis</topic><topic>Prostaglandin-Endoperoxide Synthases - genetics</topic><topic>Prostaglandins - biosynthesis</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Receptors, Prostaglandin - biosynthesis</topic><topic>Receptors, Prostaglandin - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Eva H. C</creatorcontrib><creatorcontrib>Vanhoutte, Paul M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Physiological genomics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Eva H. C</au><au>Vanhoutte, Paul M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension</atitle><jtitle>Physiological genomics</jtitle><addtitle>Physiol Genomics</addtitle><date>2008-02-19</date><risdate>2008</risdate><volume>32</volume><issue>3</issue><spage>409</spage><epage>418</epage><pages>409-418</pages><issn>1094-8341</issn><eissn>1531-2267</eissn><abstract>Department of Pharmacology, University of Hong Kong, Hong Kong
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 E 2 (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 D 2 (DP), EP 3 , and EP 4 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.
endothelium-dependent contractions; endothelium-derived contracting factors; prostacyclin synthase; prostacyclin; real-time quantitative polymerase chain reaction</abstract><cop>United States</cop><pub>Am Physiological Soc</pub><pmid>18056786</pmid><doi>10.1152/physiolgenomics.00136.2007</doi><tpages>10</tpages></addata></record> |
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| ispartof | Physiological genomics, 2008-02, Vol.32 (3), p.409-418 |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Acetylcholine - pharmacology Aging - genetics Animals Aorta, Thoracic - drug effects Cyclooxygenase 1 - biosynthesis Cyclooxygenase 1 - genetics Endothelial Cells - metabolism Enzyme Induction Gene Expression Profiling Gene Expression Regulation Hypertension - genetics Membrane Proteins - biosynthesis Membrane Proteins - genetics Muscle Proteins - biosynthesis Muscle Proteins - genetics Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Nitric Oxide Synthase Type II - biosynthesis Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type III Phenylephrine - pharmacology Prostaglandin-Endoperoxide Synthases - biosynthesis Prostaglandin-Endoperoxide Synthases - genetics Prostaglandins - biosynthesis Rats Rats, Inbred SHR Rats, Inbred WKY Receptors, Prostaglandin - biosynthesis Receptors, Prostaglandin - genetics |
| 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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