"Ca2+ Entry via TRPC1 is Essential for Cellular Differentiation and Mod" by Thad A. Rosenberger, Anne Schaar et al.
 

Document Type

Article

Publication Date

2019

Publication Title

Journal of Cell Science

Volume

132

Abstract

Adipocyte functionality, including adipocyte differentiation and adipokine secretion, is essential in obesity-associated metabolic syndrome. Here, we provide evidence that Ca2+ influx in primary adipocytes, especially upon 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 dependent on TRPC1-STIM1 and blocking Ca2+ entry with SKF-96365 or TRPC1-/- derived 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 adipocytes differentiation and adiponectin secretion, and loss of TRPC1 disturbs metabolic homeostasis.

Issue

13

DOI

10.1242/jcs.231878

ISSN

00219533

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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