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Activating of ATP-dependent K+ channels comprised of K(ir) 6.2 and SUR 2B by PGE2 through EP2 receptor in cultured interstitial cells of Cajal from murine small intestine

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dc.contributor.authorChoi, Seok-
dc.contributor.authorYeum, Cheol Ho-
dc.contributor.authorChang, In Youb-
dc.contributor.authorYou, Ho Jin-
dc.contributor.authorPark, Jong Sung-
dc.contributor.authorJeong, Han Seong-
dc.contributor.authorSo, Insuk-
dc.contributor.authorKim, Ki Whan-
dc.contributor.authorJun, Jae Yeoul-
dc.date.accessioned2010-01-07T06:36:10Z-
dc.date.available2010-01-07T06:36:10Z-
dc.date.issued2006-12-15-
dc.identifier.citationCell Physiol Biochem. 2006;18(4-5):187-98.en
dc.identifier.issn1015-8987 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17167224-
dc.identifier.urihttps://hdl.handle.net/10371/28464-
dc.description.abstractThe interstitial cells of Cajal (ICC) are pacemaker cells in gastrointestinal tract and generate an electrical rhythm in gastrointestinal muscles. We investigated the possibility that PGE(2) might affect the electrical properties of cultured ICC by activating ATP-dependent K(+) channels and, the EP receptor subtypes and the subunits of ATP-dependent K(+) channels involved in these activities were identified. In addition, the regulation of intracellular Ca(2+) ([Ca(2+)](i)) mobilization may be involved the action of PGE(2) on ICC. Treatments of ICC with PGE(2) inhibited electrical pacemaker activities in the same manner as pinacidil, an ATP-dependent K(+) channel opener and PGE(2) had only a dose-dependent effect. Using RT-PCR technique, we found that ATP-dependent K(+) channels exist in ICC and that these are composed of K(ir) 6.2 and SUR 2B subunits. To characterize the specific membrane EP receptor subtypes in ICC, EP receptor agonists and RT-PCR were used: Butaprost (an EP(2) receptor agonist) showed the actions on pacemaker currents in the same manner as PGE(2). However sulprostone (a mixed EP(1) and EP(3) agonist) had no effects. In addition, RT-PCR results indicated the presence of the EP(2) receptor in ICC. To investigate cAMP involvement in the effects of PGE(2) on ICCs, SQ-22536 (an inhibitor of adenylate cyclase) and cAMP assays were used. SQ-22536 did not affect the effect of PGE(2) on pacemaker currents, and PGE(2) did not stimulate cAMP production. Also, we found PGE(2) inhibited the spontaneous [Ca(2+)](i) oscillations in cultured ICC. These observations indicate that PGE(2) alters pacemaker currents by activating the ATP-dependent K(+) channels comprised of K(ir) 6.2-SUR 2B in ICC and this action of PGE(2) are through EP(2) receptor subtype and also the activation of ATP-dependent K(+) channels involves intracellular Ca(2+) mobilization.en
dc.language.isoenen
dc.publisherKargeren
dc.subjectATP-Binding Cassette Transporters/*agonists/analysis/geneticsen
dc.subjectAdenine/analogs & derivatives/pharmacologyen
dc.subjectAdenosine Triphosphate/metabolismen
dc.subjectAdenylate Cyclase/antagonists & inhibitorsen
dc.subjectAlprostadil/analogs & derivatives/pharmacologyen
dc.subjectAnimalsen
dc.subjectCalcium/metabolismen
dc.subjectCells, Cultureden
dc.subjectDinoprostone/*pharmacologyen
dc.subjectDose-Response Relationship, Drugen
dc.subjectElectrophysiologyen
dc.subjectFemaleen
dc.subjectIntestine, Small/chemistry/cytology/*drug effectsen
dc.subjectMaleen
dc.subjectMembrane Potentialsen
dc.subjectMiceen
dc.subjectMice, Inbred BALB Cen
dc.subjectPotassium Channels/*agonists/analysis/geneticsen
dc.subjectPotassium Channels, Inwardly Rectifying/*agonists/analysis/geneticsen
dc.subjectReceptors, Drug/*agonists/analysis/geneticsen
dc.subjectReceptors, Prostaglandin E/*metabolismen
dc.titleActivating of ATP-dependent K+ channels comprised of K(ir) 6.2 and SUR 2B by PGE2 through EP2 receptor in cultured interstitial cells of Cajal from murine small intestineen
dc.typeArticleen
dc.contributor.AlternativeAuthor최석-
dc.contributor.AlternativeAuthor염철호-
dc.contributor.AlternativeAuthor장인엽-
dc.contributor.AlternativeAuthor유호진-
dc.contributor.AlternativeAuthor박종성-
dc.contributor.AlternativeAuthor정한성-
dc.contributor.AlternativeAuthor소인숙-
dc.contributor.AlternativeAuthor김기환-
dc.contributor.AlternativeAuthor전제열-
dc.identifier.doi10.1159/000097516-
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