Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/9699
Título : Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
Autor : Schaar, Anne 
Sun, Yuyang 
Sukumaran, Pramod 
Rosenberger, Thad A. 
Krout, Danielle 
Roemmich, James N. 
Brinbaumer, Lutz 
Claycombe-Larson, Kate 
Singh, Brij B. 
Palabras clave : TRPC1SINDROME METABOLICOOBESIDADTEJIDO ADIPOSO
Fecha de publicación : 2019
Editorial : Company of Biologists
Cita : Schaar, A. et al. Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex [en línea]. Journal of Cell Science. 2019, 132. doi:10.1242/jcs.231878 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/9699
Resumen : Abstract: Properties of adipocytes, including differentiation and adipokine secretion, are crucial factors in obesity-associated metabolic syndrome. Here, we provide evidence that Ca2+ influx in primary adipocytes, especially upon Ca2+ store depletion, plays an important role in adipocyte differentiation, functionality and subsequently metabolic regulation. The endogenous Ca2+ entry channel in both subcutaneous and visceral adipocytes was found to be dependent on TRPC1-STIM1, and blocking Ca2+ entry with SKF96365 or using TRPC1-/- knockdown adipocytes inhibited adipocyte differentiation. Additionally, TRPC1-/- mice have decreased organ weight, but increased adipose deposition and reduced serum adiponectin and leptin concentrations, without affecting total adipokine expression. Mechanistically, TRPC1-mediated Ca2+ entry regulated SNARE complex formation, and agonist-mediated secretion of adipokine-loaded vesicles was inhibited in TRPC1-/- adipose. These results suggest an unequivocal role of TRPC1 in adipocyte differentiation and adiponectin secretion, and that loss of TRPC1 disturbs metabolic homeostasis.This article has an associated First Person interview with the first author of the paper.
URI : https://repositorio.uca.edu.ar/handle/123456789/9699
ISSN : 0021-9533 (impreso)
1477-9137 (online)
Disciplina: MEDICINA
DOI: 10.1242/jcs.231878
Derechos: Acceso abierto
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