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

Autores
Schaar, Anne; Sun, Yuyang; Sukumaran, Pramod; Rosenberger, Thad A.; Krout, Danielle; Roemmich, James N.; Brinbaumer, Lutz; Claycombe-Larson, Kate; Singh, Brij B.
Año de publicación
2019
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fil: Schaar, Anne. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Sun, Yuyang. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Sukumaran, Pramod. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Rosenberger, Thad A. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Krout, Danielle. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados Unidos
Fil: Roemmich, James N. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados Unidos
Fil: Brinbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos
Fil: Brinbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Claycombe-Larson, Kate. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados Unidos
Fil: Singh, Brij B. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
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.
Fuente
Journal of Cell Science. 2019, 132
Materia
TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/9699
Acceder
id RIUCA_eb2879eaa0838f05093274bd05f33992
oai_identifier_str oai:ucacris:123456789/9699
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complexSchaar, AnneSun, YuyangSukumaran, PramodRosenberger, Thad A.Krout, DanielleRoemmich, James N.Brinbaumer, LutzClaycombe-Larson, KateSingh, Brij B.TRPC1SINDROME METABOLICOOBESIDADTEJIDO ADIPOSOFil: Schaar, Anne. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados UnidosFil: Sun, Yuyang. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados UnidosFil: Sukumaran, Pramod. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados UnidosFil: Rosenberger, Thad A. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados UnidosFil: Krout, Danielle. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados UnidosFil: Roemmich, James N. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados UnidosFil: Brinbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados UnidosFil: Brinbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; ArgentinaFil: Claycombe-Larson, Kate. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados UnidosFil: Singh, Brij B. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados UnidosAbstract: 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.Company of Biologists2019info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/96990021-9533 (impreso)1477-9137 (online)10.1242/jcs.23187831182642Schaar, 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/123456789/9699Journal of Cell Science. 2019, 132reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:57:11Zoai:ucacris:123456789/9699instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:57:12.02Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
title Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
spellingShingle Ca2+ entry via TRPC1 is essential for cellular differentiation and modulates secretion via the SNARE complex
Schaar, Anne
TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
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
dc.creator.none.fl_str_mv Schaar, Anne
Sun, Yuyang
Sukumaran, Pramod
Rosenberger, Thad A.
Krout, Danielle
Roemmich, James N.
Brinbaumer, Lutz
Claycombe-Larson, Kate
Singh, Brij B.
author Schaar, Anne
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_role author
author2 Sun, Yuyang
Sukumaran, Pramod
Rosenberger, Thad A.
Krout, Danielle
Roemmich, James N.
Brinbaumer, Lutz
Claycombe-Larson, Kate
Singh, Brij B.
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
topic TRPC1
SINDROME METABOLICO
OBESIDAD
TEJIDO ADIPOSO
dc.description.none.fl_txt_mv Fil: Schaar, Anne. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Sun, Yuyang. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Sukumaran, Pramod. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Rosenberger, Thad A. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
Fil: Krout, Danielle. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados Unidos
Fil: Roemmich, James N. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados Unidos
Fil: Brinbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos
Fil: Brinbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentina
Fil: Claycombe-Larson, Kate. Grand Forks Human Nutrition Research Center. United States Department of Agriculture. Agricultural Research Service; Estados Unidos
Fil: Singh, Brij B. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
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.
description Fil: Schaar, Anne. University of North Dakota. School of Medicine and Health Sciences. Department of Biomedical Science; Estados Unidos
publishDate 2019
dc.date.none.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://repositorio.uca.edu.ar/handle/123456789/9699
0021-9533 (impreso)
1477-9137 (online)
10.1242/jcs.231878
31182642
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
url https://repositorio.uca.edu.ar/handle/123456789/9699
identifier_str_mv 0021-9533 (impreso)
1477-9137 (online)
10.1242/jcs.231878
31182642
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
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Company of Biologists
publisher.none.fl_str_mv Company of Biologists
dc.source.none.fl_str_mv Journal of Cell Science. 2019, 132
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
_version_ 1836638350466875392
score 12.982451

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