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Article: Androgen control of cyclooxygenase expression in the rat epididymis

TitleAndrogen control of cyclooxygenase expression in the rat epididymis
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. 63 n. 3, p. 775-780 How to Cite?
AbstractBradykinin and a number of peptide hormones such as angiotensin, endothelin, and vasopressin stimulate anion secretion in rat epididymis via local formation of PGE 2. These effects are mediated by cyclooxygenase (COX)-1 isozyme. The present study was undertaken to assess the androgen control of COX expression in the epididymis. Adult male Sprague-Dawley rats were bilaterally castrated through a scrotal route. Reverse transcription-polymerase chain reaction was used to measure COX-1 and COX-2 mRNAs in the epididymis in normal and castrated rats. Anion secretion in epithelia grown from the epididymides of these rats was studied by the short-circuit current technique. In normal rats, COX-1 and COX-2 mRNAs were detected in the intact epididymis. Elimination of spermatozoa by the technique of efferent duct ligation or flushing out spermatozoa did not affect the expression of either enzyme in the epididymis, indicating that the epithelium, but not spermatozoa, expressed the enzymes. Castration caused a time-dependent decrease in expression of COX-1 and COX-2 mRNAs, which were partially restored upon testosterone replacement. In epithelia cultured from castrated rats, there was a complete loss of bradykinin-induced anion secretion. This effect was reversible upon testosterone replacement. Although epithelia from castrated rats did not respond to bradykinin, they could respond to cAMP, forskolin, and PGE 2 with only 20% loss of response magnitude when compared with epithelia from normal rats. These results suggest that the expression of COX-1 and COX-2 are dependent on androgen. The loss of COX-1 expression after castration correlates with the specific loss of anion secretion induced by bradykinin and possibly other hormones.
Persistent Identifierhttp://hdl.handle.net/10722/169742
ISSN
2015 Impact Factor: 3.471
2015 SCImago Journal Rankings: 1.646
ISI Accession Number ID
References
Errata

 

DC FieldValueLanguage
dc.contributor.authorCheuk, BLYen_US
dc.contributor.authorLeung, PSen_US
dc.contributor.authorLo, ACTen_US
dc.contributor.authorWong, PYDen_US
dc.date.accessioned2012-10-25T04:54:47Z-
dc.date.available2012-10-25T04:54:47Z-
dc.date.issued2000en_US
dc.identifier.citationBiology Of Reproduction, 2000, v. 63 n. 3, p. 775-780en_US
dc.identifier.issn0006-3363en_US
dc.identifier.urihttp://hdl.handle.net/10722/169742-
dc.description.abstractBradykinin and a number of peptide hormones such as angiotensin, endothelin, and vasopressin stimulate anion secretion in rat epididymis via local formation of PGE 2. These effects are mediated by cyclooxygenase (COX)-1 isozyme. The present study was undertaken to assess the androgen control of COX expression in the epididymis. Adult male Sprague-Dawley rats were bilaterally castrated through a scrotal route. Reverse transcription-polymerase chain reaction was used to measure COX-1 and COX-2 mRNAs in the epididymis in normal and castrated rats. Anion secretion in epithelia grown from the epididymides of these rats was studied by the short-circuit current technique. In normal rats, COX-1 and COX-2 mRNAs were detected in the intact epididymis. Elimination of spermatozoa by the technique of efferent duct ligation or flushing out spermatozoa did not affect the expression of either enzyme in the epididymis, indicating that the epithelium, but not spermatozoa, expressed the enzymes. Castration caused a time-dependent decrease in expression of COX-1 and COX-2 mRNAs, which were partially restored upon testosterone replacement. In epithelia cultured from castrated rats, there was a complete loss of bradykinin-induced anion secretion. This effect was reversible upon testosterone replacement. Although epithelia from castrated rats did not respond to bradykinin, they could respond to cAMP, forskolin, and PGE 2 with only 20% loss of response magnitude when compared with epithelia from normal rats. These results suggest that the expression of COX-1 and COX-2 are dependent on androgen. The loss of COX-1 expression after castration correlates with the specific loss of anion secretion induced by bradykinin and possibly other hormones.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.meshAnimalsen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshCyclic Amp - Pharmacologyen_US
dc.subject.meshCyclooxygenase 1en_US
dc.subject.meshCyclooxygenase 2en_US
dc.subject.meshDinoprostone - Pharmacologyen_US
dc.subject.meshEpididymis - Enzymologyen_US
dc.subject.meshEpithelium - Enzymologyen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshGene Expression Regulation, Enzymologic - Drug Effectsen_US
dc.subject.meshIsoenzymes - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Proteinsen_US
dc.subject.meshOrchiectomyen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Geneticsen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTestosterone - Pharmacologyen_US
dc.titleAndrogen control of cyclooxygenase expression in the rat epididymisen_US
dc.typeArticleen_US
dc.identifier.emailCheuk, BLY: bernice@hku.hken_US
dc.identifier.authorityCheuk, BLY=rp01671en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid10952920-
dc.identifier.scopuseid_2-s2.0-0033842569en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033842569&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume63en_US
dc.identifier.issue3en_US
dc.identifier.spage775en_US
dc.identifier.epage780en_US
dc.identifier.isiWOS:000088972400016-
dc.publisher.placeUnited Statesen_US
dc.relation.erratumeid:eid_2-s2.0-0033761617-
dc.identifier.scopusauthoridCheuk, BLY=7801343617en_US
dc.identifier.scopusauthoridLeung, PS=7401748938en_US
dc.identifier.scopusauthoridLo, ACT=36800888200en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US

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