Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex

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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 differenti...

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Autores principales: Schaar, Anne, Sun, Yuyang, Sukumaran, Pramod, Rosenberger, Thad A., Krout, Danielle, Roemmich, James N., Brinbaumer, Lutz, Claycombe-Larson, Kate, Singh, Brij B.
Formato: Artículo
Lenguaje:Inglés
Publicado: Company of Biologists 2020
Materias:
TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/9699
Aporte de:
Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
id I33-R139123456789-9699
record_format dspace
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
spellingShingle TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
Schaar, Anne
Sun, Yuyang
Sukumaran, Pramod
Rosenberger, Thad A.
Krout, Danielle
Roemmich, James N.
Brinbaumer, Lutz
Claycombe-Larson, Kate
Singh, Brij B.
Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
topic_facet TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
description 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.
format Artículo
author Schaar, Anne
Sun, Yuyang
Sukumaran, Pramod
Rosenberger, Thad A.
Krout, Danielle
Roemmich, James N.
Brinbaumer, Lutz
Claycombe-Larson, Kate
Singh, Brij B.
author_facet Schaar, Anne
Sun, Yuyang
Sukumaran, Pramod
Rosenberger, Thad A.
Krout, Danielle
Roemmich, James N.
Brinbaumer, Lutz
Claycombe-Larson, Kate
Singh, Brij B.
author_sort Schaar, Anne
title Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
title_short Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
title_full Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
title_fullStr Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
title_full_unstemmed Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
title_sort ca2+ entry via trpc1 is essential for cellular differentiation and modulates secretion via the snare complex
publisher Company of Biologists
publishDate 2020
url https://repositorio.uca.edu.ar/handle/123456789/9699
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