File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: 14,15-Epoxyeicosatrienoic acid induces vasorelaxation through the prostaglandin EP2 receptors in rat mesenteric artery
  • Basic View
  • Metadata View
  • XML View
Title14,15-Epoxyeicosatrienoic acid induces vasorelaxation through the prostaglandin EP2 receptors in rat mesenteric artery
 
AuthorsYang, C1
Kwan, YW4
Au, ALS4
Poon, CCW4
Zhang, Q4
Chan, SW3
Lee, SMY2
Leung, GPH1
 
KeywordsEETs
Prostanoid
Vascular smooth muscle cells
Vasorelaxation
 
Issue Date2010
 
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/prostaglandins
 
CitationProstaglandins And Other Lipid Mediators, 2010, v. 93 n. 1-2, p. 44-51 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.prostaglandins.2010.06.004
 
AbstractEpoxyeicosatrienoic acids (EETs) induce vasorelaxation, probably through G protein-coupled receptors. The identity of these receptors is unclear, but it has been reported that EETs may bind to peroxisome proliferator activated receptors (PPARs) and E-prostanoid (EP) receptors. Therefore, we studied whether PPARs or EP receptors were involved in 14,15-EET-induced vasorelaxation. Isometric tensions of rat mesenteric arteries were measured. The vasorelaxant effect of 14,15-EET was inhibited by NF449 (Gs-protein inhibitor), Rp-cAMP (cAMP antagonist) and KT5720 (PKA inhibitor), suggesting that the effect of 14,15-EET was mediated through Gs protein-coupled receptors which were linked to the cAMP/PKA-dependent pathway. Pretreatments with MK886 (PPARα antagonist) and GW9662 (PPARγ antagonist) did not influence 14,15-EET-induced vasorelaxation. The vasorelaxant effect of 14,15-EET was inhibited by AH6809 (EP2 receptor antagonist), whereas SC19220 (EP1 receptor antagonist), L798106 (EP3 receptor antagonist) and GW627368X (EP4 receptor antagonist) had no effect. The effect of 14,15-EET and the mechanism involved was mimicked by prostaglandin E2 (an EP2 receptor agonist). The 14,15-EET-induced relaxation was slightly potentiated in the presence of indomethacin (cyclooxygenase inhibitor which block PGE2 synthesis). Binding study showed that the amount of 14,15-EET bound to the cell membrane of rat mesenteric arterial smooth muscle cells was much higher than that bound to the nuclear membrane. The binding of 14,15-EET to the cell membrane was attenuated by AH6809 and siRNA against EP2 receptors. In conclusion, our study has demonstrated that 14,15-EET exerts relaxant effects on rat mesenteric arteries, at least partly via the stimulation of EP2 receptors. This subsequently leads to activation of cAMP/PKA-dependent pathway in vascular smooth muscle cells. © 2010 Elsevier Inc.
 
ISSN1098-8823
2012 Impact Factor: 2.422
2012 SCImago Journal Rankings: 0.905
 
DOIhttp://dx.doi.org/10.1016/j.prostaglandins.2010.06.004
 
ISI Accession Number IDWOS:000281748000008
Funding AgencyGrant Number
Hong Kong SAR769607
University of Hong Kong200711159031
Funding Information:

This work was supported by the RGC Earmarked Grants of Hong Kong SAR (project code: 769607), and the Seed Funding for Basic Research Program of the University of Hong Kong (project code: 200711159031).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorYang, C
 
dc.contributor.authorKwan, YW
 
dc.contributor.authorAu, ALS
 
dc.contributor.authorPoon, CCW
 
dc.contributor.authorZhang, Q
 
dc.contributor.authorChan, SW
 
dc.contributor.authorLee, SMY
 
dc.contributor.authorLeung, GPH
 
dc.date.accessioned2011-08-26T14:26:04Z
 
dc.date.available2011-08-26T14:26:04Z
 
dc.date.issued2010
 
dc.description.abstractEpoxyeicosatrienoic acids (EETs) induce vasorelaxation, probably through G protein-coupled receptors. The identity of these receptors is unclear, but it has been reported that EETs may bind to peroxisome proliferator activated receptors (PPARs) and E-prostanoid (EP) receptors. Therefore, we studied whether PPARs or EP receptors were involved in 14,15-EET-induced vasorelaxation. Isometric tensions of rat mesenteric arteries were measured. The vasorelaxant effect of 14,15-EET was inhibited by NF449 (Gs-protein inhibitor), Rp-cAMP (cAMP antagonist) and KT5720 (PKA inhibitor), suggesting that the effect of 14,15-EET was mediated through Gs protein-coupled receptors which were linked to the cAMP/PKA-dependent pathway. Pretreatments with MK886 (PPARα antagonist) and GW9662 (PPARγ antagonist) did not influence 14,15-EET-induced vasorelaxation. The vasorelaxant effect of 14,15-EET was inhibited by AH6809 (EP2 receptor antagonist), whereas SC19220 (EP1 receptor antagonist), L798106 (EP3 receptor antagonist) and GW627368X (EP4 receptor antagonist) had no effect. The effect of 14,15-EET and the mechanism involved was mimicked by prostaglandin E2 (an EP2 receptor agonist). The 14,15-EET-induced relaxation was slightly potentiated in the presence of indomethacin (cyclooxygenase inhibitor which block PGE2 synthesis). Binding study showed that the amount of 14,15-EET bound to the cell membrane of rat mesenteric arterial smooth muscle cells was much higher than that bound to the nuclear membrane. The binding of 14,15-EET to the cell membrane was attenuated by AH6809 and siRNA against EP2 receptors. In conclusion, our study has demonstrated that 14,15-EET exerts relaxant effects on rat mesenteric arteries, at least partly via the stimulation of EP2 receptors. This subsequently leads to activation of cAMP/PKA-dependent pathway in vascular smooth muscle cells. © 2010 Elsevier Inc.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationProstaglandins And Other Lipid Mediators, 2010, v. 93 n. 1-2, p. 44-51 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.prostaglandins.2010.06.004
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.prostaglandins.2010.06.004
 
dc.identifier.epage51
 
dc.identifier.hkuros189173
 
dc.identifier.isiWOS:000281748000008
Funding AgencyGrant Number
Hong Kong SAR769607
University of Hong Kong200711159031
Funding Information:

This work was supported by the RGC Earmarked Grants of Hong Kong SAR (project code: 769607), and the Seed Funding for Basic Research Program of the University of Hong Kong (project code: 200711159031).

 
dc.identifier.issn1098-8823
2012 Impact Factor: 2.422
2012 SCImago Journal Rankings: 0.905
 
dc.identifier.issue1-2
 
dc.identifier.pmid20601071
 
dc.identifier.scopuseid_2-s2.0-77955421347
 
dc.identifier.spage44
 
dc.identifier.urihttp://hdl.handle.net/10722/137485
 
dc.identifier.volume93
 
dc.languageeng
 
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/prostaglandins
 
dc.publisher.placeUnited States
 
dc.relation.ispartofProstaglandins and Other Lipid Mediators
 
dc.relation.referencesReferences in Scopus
 
dc.subject.mesh8,11,14-Eicosatrienoic Acid - analogs and derivatives - pharmacology
 
dc.subject.meshMesenteric Arteries - drug effects - metabolism - physiology
 
dc.subject.meshReceptors, Prostaglandin E, EP2 Subtype - metabolism
 
dc.subject.meshVasodilation - drug effects
 
dc.subject.meshVasodilator Agents - pharmacology
 
dc.subjectEETs
 
dc.subjectProstanoid
 
dc.subjectVascular smooth muscle cells
 
dc.subjectVasorelaxation
 
dc.title14,15-Epoxyeicosatrienoic acid induces vasorelaxation through the prostaglandin EP2 receptors in rat mesenteric artery
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Yang, C</contributor.author>
<contributor.author>Kwan, YW</contributor.author>
<contributor.author>Au, ALS</contributor.author>
<contributor.author>Poon, CCW</contributor.author>
<contributor.author>Zhang, Q</contributor.author>
<contributor.author>Chan, SW</contributor.author>
<contributor.author>Lee, SMY</contributor.author>
<contributor.author>Leung, GPH</contributor.author>
<date.accessioned>2011-08-26T14:26:04Z</date.accessioned>
<date.available>2011-08-26T14:26:04Z</date.available>
<date.issued>2010</date.issued>
<identifier.citation>Prostaglandins And Other Lipid Mediators, 2010, v. 93 n. 1-2, p. 44-51</identifier.citation>
<identifier.issn>1098-8823</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/137485</identifier.uri>
<description.abstract>Epoxyeicosatrienoic acids (EETs) induce vasorelaxation, probably through G protein-coupled receptors. The identity of these receptors is unclear, but it has been reported that EETs may bind to peroxisome proliferator activated receptors (PPARs) and E-prostanoid (EP) receptors. Therefore, we studied whether PPARs or EP receptors were involved in 14,15-EET-induced vasorelaxation. Isometric tensions of rat mesenteric arteries were measured. The vasorelaxant effect of 14,15-EET was inhibited by NF449 (Gs-protein inhibitor), Rp-cAMP (cAMP antagonist) and KT5720 (PKA inhibitor), suggesting that the effect of 14,15-EET was mediated through Gs protein-coupled receptors which were linked to the cAMP/PKA-dependent pathway. Pretreatments with MK886 (PPAR&#945; antagonist) and GW9662 (PPAR&#947; antagonist) did not influence 14,15-EET-induced vasorelaxation. The vasorelaxant effect of 14,15-EET was inhibited by AH6809 (EP2 receptor antagonist), whereas SC19220 (EP1 receptor antagonist), L798106 (EP3 receptor antagonist) and GW627368X (EP4 receptor antagonist) had no effect. The effect of 14,15-EET and the mechanism involved was mimicked by prostaglandin E2 (an EP2 receptor agonist). The 14,15-EET-induced relaxation was slightly potentiated in the presence of indomethacin (cyclooxygenase inhibitor which block PGE2 synthesis). Binding study showed that the amount of 14,15-EET bound to the cell membrane of rat mesenteric arterial smooth muscle cells was much higher than that bound to the nuclear membrane. The binding of 14,15-EET to the cell membrane was attenuated by AH6809 and siRNA against EP2 receptors. In conclusion, our study has demonstrated that 14,15-EET exerts relaxant effects on rat mesenteric arteries, at least partly via the stimulation of EP2 receptors. This subsequently leads to activation of cAMP/PKA-dependent pathway in vascular smooth muscle cells. &#169; 2010 Elsevier Inc.</description.abstract>
<language>eng</language>
<publisher>Elsevier Inc. The Journal&apos;s web site is located at http://www.elsevier.com/locate/prostaglandins</publisher>
<relation.ispartof>Prostaglandins and Other Lipid Mediators</relation.ispartof>
<subject>EETs</subject>
<subject>Prostanoid</subject>
<subject>Vascular smooth muscle cells</subject>
<subject>Vasorelaxation</subject>
<subject.mesh>8,11,14-Eicosatrienoic Acid - analogs and derivatives - pharmacology</subject.mesh>
<subject.mesh>Mesenteric Arteries - drug effects - metabolism - physiology</subject.mesh>
<subject.mesh>Receptors, Prostaglandin E, EP2 Subtype - metabolism</subject.mesh>
<subject.mesh>Vasodilation - drug effects</subject.mesh>
<subject.mesh>Vasodilator Agents - pharmacology</subject.mesh>
<title>14,15-Epoxyeicosatrienoic acid induces vasorelaxation through the prostaglandin EP2 receptors in rat mesenteric artery</title>
<type>Article</type>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1016/j.prostaglandins.2010.06.004</identifier.doi>
<identifier.pmid>20601071</identifier.pmid>
<identifier.scopus>eid_2-s2.0-77955421347</identifier.scopus>
<identifier.hkuros>189173</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-77955421347&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>93</identifier.volume>
<identifier.issue>1-2</identifier.issue>
<identifier.spage>44</identifier.spage>
<identifier.epage>51</identifier.epage>
<identifier.isi>WOS:000281748000008</identifier.isi>
<publisher.place>United States</publisher.place>
</item>
Author Affiliations
  1. The University of Hong Kong
  2. University of Macau
  3. Hong Kong Polytechnic University
  4. Chinese University of Hong Kong