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dc.creatorSun, Yuyang-
dc.creatorBirnbaumer, Lutz-
dc.creatorSingh, Brij B.-
dc.date2018-03-05T19:27:15Z-
dc.date2018-03-05T19:27:15Z-
dc.date2015-11-
dc.date2018-03-02T17:33:08Z-
dc.date.accessioned2019-04-29T15:53:25Z-
dc.date.available2019-04-29T15:53:25Z-
dc.date.issued2015-11-
dc.identifierSun, Yuyang; Birnbaumer, Lutz; Singh, Brij B.; TRPC1 regulates calcium-activated chloride channels in salivary gland cells; Wiley-liss, Div John Wiley & Sons Inc; Journal of Cellular Physiology; 230; 11; 11-2015; 2848-2856-
dc.identifier0021-9541-
dc.identifierhttp://hdl.handle.net/11336/37875-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/304745-
dc.descriptionCalcium-activated chloride channel (CaCC) plays an important role in modulating epithelial secretion. It has been suggested that in salivary tissues, sustained fluid secretion is dependent on Ca2+ influx that activates ion channels such as CaCC to initiate Cl- efflux. However direct evidence as well as the molecular identity of the Ca2+ channel responsible for activating CaCC in salivary tissues is not yet identified. Here we provide evidence that in human salivary cells, an outward rectifying Cl- current was activated by increasing [Ca2+]i, which was inhibited by the addition of pharmacological agents niflumic acid (NFA), an antagonist of CaCC, or T16Ainh-A01, a specific TMEM16a inhibitor. Addition of thapsigargin (Tg), that induces store-depletion and activates TRPC1-mediated Ca2+ entry, potentiated the Cl- current, which was inhibited by the addition of a non-specific TRPC channel blocker SKF96365 or removal of external Ca2+. Stimulation with Tg also increased plasma membrane expression of TMEM16a protein, which was also dependent on Ca2+ entry. Importantly, in salivary cells, TRPC1 silencing, but not that of TRPC3, inhibited CaCC especially upon store depletion. Moreover, primary acinar cells isolated from submandibular gland also showed outward rectifying Cl- currents upon increasing [Ca2+]i. These Cl- currents were again potentiated with the addition of Tg, but inhibited in the presence of T16Ainh-A01. Finally, acinar cells isolated from the submandibular glands of TRPC1 knockout mice showed significant inhibition of the outward Cl- currents without decreasing TMEM16a expression. Together the data suggests that Ca2+ entry via the TRPC1 channels is essential for the activation of CaCC.-
dc.descriptionFil: Sun, Yuyang. University Of North Dakota; Estados Unidos-
dc.descriptionFil: Birnbaumer, Lutz. National Institutes of Health; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina-
dc.descriptionFil: Singh, Brij B.. University Of North Dakota; Estados Unidos-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherWiley-liss, Div John Wiley & Sons Inc-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1002/jcp.25017-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/jcp.25017/abstract-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.subjectTMEM6a-
dc.subjectTRPC1-
dc.subjectsalivary gland-
dc.subjectCa activated chloride channel-
dc.subjectOtras Ciencias Biológicas-
dc.subjectCiencias Biológicas-
dc.subjectCIENCIAS NATURALES Y EXACTAS-
dc.titleTRPC1 regulates calcium-activated chloride channels in salivary gland cells-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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