Ousingsawat, Jiraporn and Martins, Joana R. and Schreiber, Rainer and Rock, Jason R. and Harfe, Brian D. and Kunzelmann, Karl (2009) Loss of TMEM16A Causes a Defect in Epithelial Ca2+-dependent Chloride Transport. JOURNAL OF BIOLOGICAL CHEMISTRY, 284 (42). pp. 28698-28703. ISSN 0021-9258, 1083-351X
Full text not available from this repository. (Request a copy)Abstract
Molecular identification of the Ca2+-dependent chloride channel TMEM16A (ANO1) provided a fundamental step in understanding Ca2+-dependent Cl- secretion in epithelia. TMEM16A is an intrinsic constituent of Ca2+-dependent Cl- channels in cultured epithelia and may control salivary output, but its physiological role in native epithelial tissues remains largely obscure. Here, we demonstrate that Cl- secretion in native epithelia activated by Ca2+-dependent agonists is missing in mice lacking expression of TMEM16A. Ca2+-dependent Cl- transport was missing or largely reduced in isolated tracheal and colonic epithelia, as well as hepatocytes and acinar cells from pancreatic and submandibular glands of TMEM16A(-/-) animals. Measurement of particle transport on the surface of tracheas ex vivo indicated largely reduced mucociliary clearance in TMEM16A(-/-) mice. These results clearly demonstrate the broad physiological role of TMEM16A(-/-) for Ca2+-dependent Cl- secretion and provide the basis for novel treatments in cystic fibrosis, infectious diarrhea, and Sjoegren syndrome.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | AGE-DEPENDENT DIARRHEA; CYSTIC-FIBROSIS; MOUSE AIRWAYS; CHANNEL; CELLS; SECRETION; MEMBRANE; GLANDS; CA2+; HEPATOCYTES; |
| Subjects: | 500 Science > 570 Life sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Karl Kunzelmann |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 03 Sep 2020 07:03 |
| Last Modified: | 03 Sep 2020 07:03 |
| URI: | https://pred.uni-regensburg.de/id/eprint/28266 |
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