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Article: Synergistic effects of cystic fibrosis transmembrane conductance regulator and aquaporin-9 in the rat epididymis

TitleSynergistic effects of cystic fibrosis transmembrane conductance regulator and aquaporin-9 in the rat epididymis
Authors
KeywordsAquaporin-9
Cystic fibrosis transmembrane conductance regulator
Epididymis
Issue Date2003
PublisherSociety for the Study of Reproduction. The Journal's web site is located at http://www.biolreprod.org/
Citation
Biology Of Reproduction, 2003, v. 68 n. 5, p. 1505-1510 How to Cite?
AbstractThe cystic fibrosis transmembrane conductance regulator (CFTR) and aquaporin-9 (AQP-9) are present in the luminal membrane of the epididymis, where they play an important role in formation of the epididymal fluid. Evidence is accumulating that CFTR regulates other membrane transport proteins besides functioning as a cAMP-activated chloride channel. We have explored the possible interaction between epididymal CFTR and AQP-9 by cloning them from the rat epididymis and expressing them in Xenopus oocytes. The effects of the expressed proteins on oocyte water permeability were studied by immersing oocytes in a hypo-osmotic solution, and the ensuing water flow was measured using a gravimetric method. The results show that AQP-9 alone caused an increase in oocyte water permeability, which could be further potentiated by CFTR. This potentiation was markedly reduced by phloretin and Ionidamine (inhibitors of AQP-9 and CFTR, respectively). The regulation of water permeability by CFTR was also demonstrated in intact rat epididymis luminally perfused with a hypo-osmotic solution. Osmotic water reabsorption across the epididymal tubule was reduced by phloretin and Ionidamine. Elevation of intracellular cAMP with 3-isobutyl-1-methylxanthine increased osmotic water permeability, whereas inhibiting protein kinase A with H-89 (N-(2- [p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide hydrochloride) reduced it. These results are consistent with a role for CFTR in controlling water permeability in the epididymis in vivo. We conclude that this additional role of CFTR in controlling water permeability may have an impact on the genetic disease cystic fibrosis, in which men with a mutated CFTR gene have abnormal epididymis and infertility.
Persistent Identifierhttp://hdl.handle.net/10722/171292
ISSN
2021 Impact Factor: 4.161
2020 SCImago Journal Rankings: 1.366
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, KHen_US
dc.contributor.authorLeung, CTen_US
dc.contributor.authorLeung, GPHen_US
dc.contributor.authorWong, PYDen_US
dc.date.accessioned2012-10-30T06:13:13Z-
dc.date.available2012-10-30T06:13:13Z-
dc.date.issued2003en_US
dc.identifier.citationBiology Of Reproduction, 2003, v. 68 n. 5, p. 1505-1510en_US
dc.identifier.issn0006-3363en_US
dc.identifier.urihttp://hdl.handle.net/10722/171292-
dc.description.abstractThe cystic fibrosis transmembrane conductance regulator (CFTR) and aquaporin-9 (AQP-9) are present in the luminal membrane of the epididymis, where they play an important role in formation of the epididymal fluid. Evidence is accumulating that CFTR regulates other membrane transport proteins besides functioning as a cAMP-activated chloride channel. We have explored the possible interaction between epididymal CFTR and AQP-9 by cloning them from the rat epididymis and expressing them in Xenopus oocytes. The effects of the expressed proteins on oocyte water permeability were studied by immersing oocytes in a hypo-osmotic solution, and the ensuing water flow was measured using a gravimetric method. The results show that AQP-9 alone caused an increase in oocyte water permeability, which could be further potentiated by CFTR. This potentiation was markedly reduced by phloretin and Ionidamine (inhibitors of AQP-9 and CFTR, respectively). The regulation of water permeability by CFTR was also demonstrated in intact rat epididymis luminally perfused with a hypo-osmotic solution. Osmotic water reabsorption across the epididymal tubule was reduced by phloretin and Ionidamine. Elevation of intracellular cAMP with 3-isobutyl-1-methylxanthine increased osmotic water permeability, whereas inhibiting protein kinase A with H-89 (N-(2- [p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide hydrochloride) reduced it. These results are consistent with a role for CFTR in controlling water permeability in the epididymis in vivo. We conclude that this additional role of CFTR in controlling water permeability may have an impact on the genetic disease cystic fibrosis, in which men with a mutated CFTR gene have abnormal epididymis and infertility.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.subjectAquaporin-9-
dc.subjectCystic fibrosis transmembrane conductance regulator-
dc.subjectEpididymis-
dc.subject.meshAbsorptionen_US
dc.subject.meshAlgorithmsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAquaporins - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshCell Membrane Permeability - Drug Effectsen_US
dc.subject.meshChloride Channels - Metabolismen_US
dc.subject.meshCloning, Molecularen_US
dc.subject.meshCyclic Amp-Dependent Protein Kinases - Metabolismen_US
dc.subject.meshCystic Fibrosis Transmembrane Conductance Regulator - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshEpididymis - Cytology - Metabolismen_US
dc.subject.meshIndazoles - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMicroinjectionsen_US
dc.subject.meshOocytes - Metabolismen_US
dc.subject.meshOsmosisen_US
dc.subject.meshPhloretin - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshXenopus Laevisen_US
dc.titleSynergistic effects of cystic fibrosis transmembrane conductance regulator and aquaporin-9 in the rat epididymisen_US
dc.typeArticleen_US
dc.identifier.emailCheung, KH:kingho.cheung@hku.hken_US
dc.identifier.emailLeung, GPH:gphleung@hkucc.hku.hken_US
dc.identifier.authorityCheung, KH=rp01463en_US
dc.identifier.authorityLeung, GPH=rp00234en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1095/biolreprod.102.010017en_US
dc.identifier.pmid12606488-
dc.identifier.scopuseid_2-s2.0-0037407445en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037407445&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume68en_US
dc.identifier.issue5en_US
dc.identifier.spage1505en_US
dc.identifier.epage1510en_US
dc.identifier.isiWOS:000182589700005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCheung, KH=14007487800en_US
dc.identifier.scopusauthoridLeung, CT=7402612664en_US
dc.identifier.scopusauthoridLeung, GPH=35963668200en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US
dc.identifier.issnl0006-3363-

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