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Article: cAMP- but not Ca 2+-regulated Cl - conductance in the oviduct is defective in mouse model of cystic fibrosis

TitlecAMP- but not Ca 2+-regulated Cl - conductance in the oviduct is defective in mouse model of cystic fibrosis
Authors
Issue Date1995
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 1995, v. 268 n. 3 37-3, p. C708-C712 How to Cite?
AbstractDefective adenosine 3',5'-cyclic monophosphate (cAMP)-mediated Cl - transport in cystic fibrosis (CF) reflects defects in the cystic fibrosis transmembrane conductance regulator (CFTR). A moderate level of CFTR mRNA expression has been found in rodent and human oviductal epithelium, but unlike other CFTR-expressing tissues, the oviduct in CF patients is apparently normal. The present study was carried out to investigate the relative magnitude of the cAMP- and intracellular Ca 2+ (Ca(i)/ 2+)- regulated Cl - secretion in primary cultures of the oviduct from normal and CF mice generated by targeted disruption of the murine CF gene. Normal oviductal epithelium exhibited a basal equivalent short-circuit current (I(eq)) of 20.3 ± 1.7 μA/cm 2. CF oviduct exhibited a lower basal I(eq) of 4.5 ± 1.9 μA/cm 2. In normal mice, forskolin (10 -5 M, apical) elicited a slowly developing sustained rise in I(eq), whereas ionomycin (5 x 10 -6 M, apical) and ATP (10 -4 M, apical) induced larger increases in I(eq) consisting of a prompt, transient response followed by a slowly decreasing component. The I(eq) response to forskolin was totally abolished in CF mouse oviducts, but the magnitudes of the peak I(eq) responses to ionomycin and ATP were not different from normal. The time courses of the ionomycin- and ATP- evoked responses, however, were significantly more transient in CF than in normal oviducts. These results demonstrate that CF mouse oviduct exhibits defective cAMP- but not Ca(i)/ 2+-mediated Cl - secretion. The relatively high level of functional expression of the alternative Ca 2+-activated Cl - secretory pathway in the mouse oviduct may contribute to the absence of major pathology in the CF oviduct.
Persistent Identifierhttp://hdl.handle.net/10722/162079
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893

 

DC FieldValueLanguage
dc.contributor.authorLeung, AYHen_US
dc.contributor.authorWong, PYDen_US
dc.contributor.authorGabriel, SEen_US
dc.contributor.authorYankaskas, JRen_US
dc.contributor.authorBoucher, RCen_US
dc.date.accessioned2012-09-05T05:17:06Z-
dc.date.available2012-09-05T05:17:06Z-
dc.date.issued1995en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 1995, v. 268 n. 3 37-3, p. C708-C712en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/162079-
dc.description.abstractDefective adenosine 3',5'-cyclic monophosphate (cAMP)-mediated Cl - transport in cystic fibrosis (CF) reflects defects in the cystic fibrosis transmembrane conductance regulator (CFTR). A moderate level of CFTR mRNA expression has been found in rodent and human oviductal epithelium, but unlike other CFTR-expressing tissues, the oviduct in CF patients is apparently normal. The present study was carried out to investigate the relative magnitude of the cAMP- and intracellular Ca 2+ (Ca(i)/ 2+)- regulated Cl - secretion in primary cultures of the oviduct from normal and CF mice generated by targeted disruption of the murine CF gene. Normal oviductal epithelium exhibited a basal equivalent short-circuit current (I(eq)) of 20.3 ± 1.7 μA/cm 2. CF oviduct exhibited a lower basal I(eq) of 4.5 ± 1.9 μA/cm 2. In normal mice, forskolin (10 -5 M, apical) elicited a slowly developing sustained rise in I(eq), whereas ionomycin (5 x 10 -6 M, apical) and ATP (10 -4 M, apical) induced larger increases in I(eq) consisting of a prompt, transient response followed by a slowly decreasing component. The I(eq) response to forskolin was totally abolished in CF mouse oviducts, but the magnitudes of the peak I(eq) responses to ionomycin and ATP were not different from normal. The time courses of the ionomycin- and ATP- evoked responses, however, were significantly more transient in CF than in normal oviducts. These results demonstrate that CF mouse oviduct exhibits defective cAMP- but not Ca(i)/ 2+-mediated Cl - secretion. The relatively high level of functional expression of the alternative Ca 2+-activated Cl - secretory pathway in the mouse oviduct may contribute to the absence of major pathology in the CF oviduct.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_US
dc.subject.meshAdenosine Triphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCalcium - Pharmacologyen_US
dc.subject.meshChloride Channels - Drug Effects - Physiologyen_US
dc.subject.meshChlorides - Metabolismen_US
dc.subject.meshCyclic Amp - Pharmacologyen_US
dc.subject.meshCystic Fibrosis - Physiopathologyen_US
dc.subject.meshCystic Fibrosis Transmembrane Conductance Regulatoren_US
dc.subject.meshElectric Conductivityen_US
dc.subject.meshFallopian Tubes - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIonomycin - Pharmacologyen_US
dc.subject.meshKineticsen_US
dc.subject.meshMembrane Proteins - Physiologyen_US
dc.subject.meshMiceen_US
dc.titlecAMP- but not Ca 2+-regulated Cl - conductance in the oviduct is defective in mouse model of cystic fibrosisen_US
dc.typeArticleen_US
dc.identifier.emailLeung, AYH:ayhleung@hku.hken_US
dc.identifier.authorityLeung, AYH=rp00265en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid7534985-
dc.identifier.scopuseid_2-s2.0-0028925784en_US
dc.identifier.volume268en_US
dc.identifier.issue3 37-3en_US
dc.identifier.spageC708en_US
dc.identifier.epageC712en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, AYH=7403012668en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US
dc.identifier.scopusauthoridGabriel, SE=7202103831en_US
dc.identifier.scopusauthoridYankaskas, JR=7005074361en_US
dc.identifier.scopusauthoridBoucher, RC=7202772816en_US

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