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Article: Activation of cystic fibrosis transmembrane conductance regulator in rat epididymal epithelium by genistein

TitleActivation of cystic fibrosis transmembrane conductance regulator in rat epididymal epithelium by genistein
Authors
Issue Date2000
PublisherSociety for the Study of Reproduction. The Journal's web site is located at http://www.biolreprod.org/
Citation
Biology Of Reproduction, 2000, v. 62 n. 1, p. 143-149 How to Cite?
AbstractThe effect of genistein on anion secretion via cystic fibrosis transmembrane conductance regulator (CFTR) in cultured rat cauda epididymal epithelia was studied by short-circuit current (Isc) technique. Genistein added apically stimulated a concentration-dependent rise in Isc due to Cl- and HCO3 - secretion. The genistein-induced Isc was observed in basolaterally permeabilized monolayers, suggesting that the Isc response was mediated by the apical anion channel. The response could be blocked by the nonspecific Cl- channel blocker, diphenylamine-2-carboxylate (DPC), but not by the Ca2+-activated Cl- channel blocker, 4,4'-diisothiocyanostilbene- 2,2'-disulfonic acid (DIDS). Genistein did not increase intracellular cAMP, but H-89, a protein kinase A inhibitor, completely abolished the Isc response to genistein. Moreover, pretreatment of the tissues with MDL-12330A, an adenylate cyclase inhibitor, markedly attenuated the Isc response to genistein, but the response was restored upon the addition of exogenous cAMP. Ca2+, protein kinase C, tyrosine kinase, and protein phosphatase signalling pathways were not involved in the action of genistein. It is speculated that genistein stimulates anion secretion by direct interaction with CFTR. This requires a low level of phosphorylation of CFTR by basal protein kinase A activity. It is suggested that genistein may provide therapeutic benefit to male infertility associated with cystic fibrosis.
Persistent Identifierhttp://hdl.handle.net/10722/171237
ISSN
2015 Impact Factor: 3.471
2015 SCImago Journal Rankings: 1.646
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, GPHen_US
dc.contributor.authorWong, PYDen_US
dc.date.accessioned2012-10-30T06:12:52Z-
dc.date.available2012-10-30T06:12:52Z-
dc.date.issued2000en_US
dc.identifier.citationBiology Of Reproduction, 2000, v. 62 n. 1, p. 143-149en_US
dc.identifier.issn0006-3363en_US
dc.identifier.urihttp://hdl.handle.net/10722/171237-
dc.description.abstractThe effect of genistein on anion secretion via cystic fibrosis transmembrane conductance regulator (CFTR) in cultured rat cauda epididymal epithelia was studied by short-circuit current (Isc) technique. Genistein added apically stimulated a concentration-dependent rise in Isc due to Cl- and HCO3 - secretion. The genistein-induced Isc was observed in basolaterally permeabilized monolayers, suggesting that the Isc response was mediated by the apical anion channel. The response could be blocked by the nonspecific Cl- channel blocker, diphenylamine-2-carboxylate (DPC), but not by the Ca2+-activated Cl- channel blocker, 4,4'-diisothiocyanostilbene- 2,2'-disulfonic acid (DIDS). Genistein did not increase intracellular cAMP, but H-89, a protein kinase A inhibitor, completely abolished the Isc response to genistein. Moreover, pretreatment of the tissues with MDL-12330A, an adenylate cyclase inhibitor, markedly attenuated the Isc response to genistein, but the response was restored upon the addition of exogenous cAMP. Ca2+, protein kinase C, tyrosine kinase, and protein phosphatase signalling pathways were not involved in the action of genistein. It is speculated that genistein stimulates anion secretion by direct interaction with CFTR. This requires a low level of phosphorylation of CFTR by basal protein kinase A activity. It is suggested that genistein may provide therapeutic benefit to male infertility associated with cystic fibrosis.en_US
dc.languageengen_US
dc.publisherSociety for the Study of Reproduction. The Journal's web site is located at http://www.biolreprod.org/en_US
dc.relation.ispartofBiology of Reproductionen_US
dc.subject.mesh4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - Pharmacologyen_US
dc.subject.meshAdenylate Cyclase - Antagonists & Inhibitorsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnthranilic Acids - Pharmacologyen_US
dc.subject.meshBicarbonates - Metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChloride Channels - Antagonists & Inhibitorsen_US
dc.subject.meshChlorides - Metabolismen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshCystic Fibrosis Transmembrane Conductance Regulator - Metabolismen_US
dc.subject.meshElectric Conductivityen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshEpididymis - Metabolismen_US
dc.subject.meshEpithelium - Metabolismen_US
dc.subject.meshGenistein - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshProtein Kinase Inhibitorsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshThapsigargin - Pharmacologyen_US
dc.titleActivation of cystic fibrosis transmembrane conductance regulator in rat epididymal epithelium by genisteinen_US
dc.typeArticleen_US
dc.identifier.emailLeung, GPH:gphleung@hkucc.hku.hken_US
dc.identifier.authorityLeung, GPH=rp00234en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1095/biolreprod62.1.143-
dc.identifier.pmid10611078-
dc.identifier.scopuseid_2-s2.0-0033962314en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033962314&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume62en_US
dc.identifier.issue1en_US
dc.identifier.spage143en_US
dc.identifier.epage149en_US
dc.identifier.isiWOS:000084401500019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, GPH=35963668200en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US

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