Journal
EMBO REPORTS
Volume 14, Issue 12, Pages 1143-1148Publisher
WILEY
DOI: 10.1038/embor.2013.170
Keywords
Fam38A; kidney; Piezo1; PKD; mechanotransduction; TRP channels
Categories
Funding
- ANR Du gene a la physiopathologie
- des maladies rares aux maladies communes
- ANR Physiologie, physiopathologie, sante publique
- Fondation de la recherche medicale
- Fondation de recherche sur l'hypertension arterielle
- Fondation de France
- Association Francaise contre les Myopathies
- Association pour l'information et la recherche sur les maladies renales genetiques France
- Region Provence Alpes Cote d'Azur
- Societe Francaise d'hypertension arterielle
- Universite de Nice Sophia Antipolis
- Centre National de la Recherche Scientifique
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Mechanical forces associated with fluid flow and/or circumferential stretch are sensed by renal epithelial cells and contribute to both adaptive or disease states. Non-selective stretch-activated ion channels (SACs), characterized by a lack of inactivation and a remarkably slow deactivation, are active at the basolateral side of renal proximal convoluted tubules. Knockdown of Piezo1 strongly reduces SAC activity in proximal convoluted tubule epithelial cells. Similarly, overexpression of Polycystin-2 (PC2) or, to a greater extent its pathogenic mutant PC2-740X, impairs native SACs. Moreover, PC2 inhibits exogenous Piezo1 SAC activity. PC2 coimmunoprecipitates with Piezo1 and deletion of its N-terminal domain prevents both this interaction and inhibition of SAC activity. These findings indicate that renal SACs depend on Piezo1, but are critically conditioned by PC2.
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