Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli

Autores
Ilatovskaya, Daria V.; Palygin, Oleg; Chubinskiy Nadezhdin, Vladislav; Negulyaev, Yuri A.; Ma, Rong; Birnbaumer, Lutz; Staruschenko, Alexander
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
A key role for podocytes in the pathogenesis of proteinuric renal diseases has been established. Angiotensin II causes depolarization and increased intracellular calcium concentration in podocytes; members of the cation TRPC channels family, particularly TRPC6, are proposed as proteins responsible for calcium flux. Angiotensin II evokes calcium transient through TRPC channels and mutations in the gene encoding the TRPC6 channel result in the development of focal segmental glomerulosclerosis. Here we examined the effects of angiotensin II on intracellular calcium ion levels and endogenous channels in intact podocytes of freshly isolated decapsulated mouse glomeruli. An ion channel with distinct TRPC6 properties was identified in wild-type, but was absent in TRPC6 knockout mice. Single-channel electrophysiological analysis found that angiotensin II acutely activated native TRPC-like channels in both podocytes of freshly isolated glomeruli and TRPC6 channels transiently overexpressed in CHO cells; the effect was mediated by changes in the channel open probability. Angiotensin II evoked intracellular calcium transients in the wild-type podocytes, which was blunted in TRPC6 knockout glomeruli. Pan-TRPC inhibitors gadolinium and SKF 96365 reduced the response in wild-type glomerular epithelial cells, whereas the transient in TRPC6 knockout animals was not affected. Thus, angiotensin II-dependent activation of TRPC6 channels in podocytes may have a significant role in the development of kidney diseases.
Fil: Ilatovskaya, Daria V.. Medical College Of Wisconsin; Estados Unidos. Russian Academy of Sciences; Rusia
Fil: Palygin, Oleg. Medical College Of Wisconsin; Estados Unidos
Fil: Chubinskiy Nadezhdin, Vladislav. Russian Academy of Sciences; Rusia
Fil: Negulyaev, Yuri A.. Russian Academy of Sciences; Rusia. St. Petersburg State Polytechnical University; Rusia
Fil: Ma, Rong. University of North Texas; Estados Unidos
Fil: Birnbaumer, Lutz. National Institutes of Health; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Staruschenko, Alexander. Medical College Of Wisconsin; Estados Unidos
Materia
ANGIOTENSIN
CALCIUM
FOCAL SEGMENTAL GLOMERULOSCLEROSIS
ION CHANNEL
NEPHROTIC SYNDROME
PODOCYTE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/95594

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network_name_str CONICET Digital (CONICET)
spelling Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruliIlatovskaya, Daria V.Palygin, OlegChubinskiy Nadezhdin, VladislavNegulyaev, Yuri A.Ma, RongBirnbaumer, LutzStaruschenko, AlexanderANGIOTENSINCALCIUMFOCAL SEGMENTAL GLOMERULOSCLEROSISION CHANNELNEPHROTIC SYNDROMEPODOCYTEhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1A key role for podocytes in the pathogenesis of proteinuric renal diseases has been established. Angiotensin II causes depolarization and increased intracellular calcium concentration in podocytes; members of the cation TRPC channels family, particularly TRPC6, are proposed as proteins responsible for calcium flux. Angiotensin II evokes calcium transient through TRPC channels and mutations in the gene encoding the TRPC6 channel result in the development of focal segmental glomerulosclerosis. Here we examined the effects of angiotensin II on intracellular calcium ion levels and endogenous channels in intact podocytes of freshly isolated decapsulated mouse glomeruli. An ion channel with distinct TRPC6 properties was identified in wild-type, but was absent in TRPC6 knockout mice. Single-channel electrophysiological analysis found that angiotensin II acutely activated native TRPC-like channels in both podocytes of freshly isolated glomeruli and TRPC6 channels transiently overexpressed in CHO cells; the effect was mediated by changes in the channel open probability. Angiotensin II evoked intracellular calcium transients in the wild-type podocytes, which was blunted in TRPC6 knockout glomeruli. Pan-TRPC inhibitors gadolinium and SKF 96365 reduced the response in wild-type glomerular epithelial cells, whereas the transient in TRPC6 knockout animals was not affected. Thus, angiotensin II-dependent activation of TRPC6 channels in podocytes may have a significant role in the development of kidney diseases.Fil: Ilatovskaya, Daria V.. Medical College Of Wisconsin; Estados Unidos. Russian Academy of Sciences; RusiaFil: Palygin, Oleg. Medical College Of Wisconsin; Estados UnidosFil: Chubinskiy Nadezhdin, Vladislav. Russian Academy of Sciences; RusiaFil: Negulyaev, Yuri A.. Russian Academy of Sciences; Rusia. St. Petersburg State Polytechnical University; RusiaFil: Ma, Rong. University of North Texas; Estados UnidosFil: Birnbaumer, Lutz. National Institutes of Health; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Staruschenko, Alexander. Medical College Of Wisconsin; Estados UnidosNature Publishing Group2014-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/95594Ilatovskaya, Daria V.; Palygin, Oleg; Chubinskiy Nadezhdin, Vladislav; Negulyaev, Yuri A.; Ma, Rong; et al.; Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli; Nature Publishing Group; Kidney International; 86; 3; 9-2014; 506-5140085-2538CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0085253815303240info:eu-repo/semantics/altIdentifier/doi/10.1038/ki.2014.71info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:04:09Zoai:ri.conicet.gov.ar:11336/95594instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-10 13:04:10.059CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
title Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
spellingShingle Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
Ilatovskaya, Daria V.
ANGIOTENSIN
CALCIUM
FOCAL SEGMENTAL GLOMERULOSCLEROSIS
ION CHANNEL
NEPHROTIC SYNDROME
PODOCYTE
title_short Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
title_full Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
title_fullStr Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
title_full_unstemmed Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
title_sort Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli
dc.creator.none.fl_str_mv Ilatovskaya, Daria V.
Palygin, Oleg
Chubinskiy Nadezhdin, Vladislav
Negulyaev, Yuri A.
Ma, Rong
Birnbaumer, Lutz
Staruschenko, Alexander
author Ilatovskaya, Daria V.
author_facet Ilatovskaya, Daria V.
Palygin, Oleg
Chubinskiy Nadezhdin, Vladislav
Negulyaev, Yuri A.
Ma, Rong
Birnbaumer, Lutz
Staruschenko, Alexander
author_role author
author2 Palygin, Oleg
Chubinskiy Nadezhdin, Vladislav
Negulyaev, Yuri A.
Ma, Rong
Birnbaumer, Lutz
Staruschenko, Alexander
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv ANGIOTENSIN
CALCIUM
FOCAL SEGMENTAL GLOMERULOSCLEROSIS
ION CHANNEL
NEPHROTIC SYNDROME
PODOCYTE
topic ANGIOTENSIN
CALCIUM
FOCAL SEGMENTAL GLOMERULOSCLEROSIS
ION CHANNEL
NEPHROTIC SYNDROME
PODOCYTE
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv A key role for podocytes in the pathogenesis of proteinuric renal diseases has been established. Angiotensin II causes depolarization and increased intracellular calcium concentration in podocytes; members of the cation TRPC channels family, particularly TRPC6, are proposed as proteins responsible for calcium flux. Angiotensin II evokes calcium transient through TRPC channels and mutations in the gene encoding the TRPC6 channel result in the development of focal segmental glomerulosclerosis. Here we examined the effects of angiotensin II on intracellular calcium ion levels and endogenous channels in intact podocytes of freshly isolated decapsulated mouse glomeruli. An ion channel with distinct TRPC6 properties was identified in wild-type, but was absent in TRPC6 knockout mice. Single-channel electrophysiological analysis found that angiotensin II acutely activated native TRPC-like channels in both podocytes of freshly isolated glomeruli and TRPC6 channels transiently overexpressed in CHO cells; the effect was mediated by changes in the channel open probability. Angiotensin II evoked intracellular calcium transients in the wild-type podocytes, which was blunted in TRPC6 knockout glomeruli. Pan-TRPC inhibitors gadolinium and SKF 96365 reduced the response in wild-type glomerular epithelial cells, whereas the transient in TRPC6 knockout animals was not affected. Thus, angiotensin II-dependent activation of TRPC6 channels in podocytes may have a significant role in the development of kidney diseases.
Fil: Ilatovskaya, Daria V.. Medical College Of Wisconsin; Estados Unidos. Russian Academy of Sciences; Rusia
Fil: Palygin, Oleg. Medical College Of Wisconsin; Estados Unidos
Fil: Chubinskiy Nadezhdin, Vladislav. Russian Academy of Sciences; Rusia
Fil: Negulyaev, Yuri A.. Russian Academy of Sciences; Rusia. St. Petersburg State Polytechnical University; Rusia
Fil: Ma, Rong. University of North Texas; Estados Unidos
Fil: Birnbaumer, Lutz. National Institutes of Health; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Staruschenko, Alexander. Medical College Of Wisconsin; Estados Unidos
description A key role for podocytes in the pathogenesis of proteinuric renal diseases has been established. Angiotensin II causes depolarization and increased intracellular calcium concentration in podocytes; members of the cation TRPC channels family, particularly TRPC6, are proposed as proteins responsible for calcium flux. Angiotensin II evokes calcium transient through TRPC channels and mutations in the gene encoding the TRPC6 channel result in the development of focal segmental glomerulosclerosis. Here we examined the effects of angiotensin II on intracellular calcium ion levels and endogenous channels in intact podocytes of freshly isolated decapsulated mouse glomeruli. An ion channel with distinct TRPC6 properties was identified in wild-type, but was absent in TRPC6 knockout mice. Single-channel electrophysiological analysis found that angiotensin II acutely activated native TRPC-like channels in both podocytes of freshly isolated glomeruli and TRPC6 channels transiently overexpressed in CHO cells; the effect was mediated by changes in the channel open probability. Angiotensin II evoked intracellular calcium transients in the wild-type podocytes, which was blunted in TRPC6 knockout glomeruli. Pan-TRPC inhibitors gadolinium and SKF 96365 reduced the response in wild-type glomerular epithelial cells, whereas the transient in TRPC6 knockout animals was not affected. Thus, angiotensin II-dependent activation of TRPC6 channels in podocytes may have a significant role in the development of kidney diseases.
publishDate 2014
dc.date.none.fl_str_mv 2014-09
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 http://hdl.handle.net/11336/95594
Ilatovskaya, Daria V.; Palygin, Oleg; Chubinskiy Nadezhdin, Vladislav; Negulyaev, Yuri A.; Ma, Rong; et al.; Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli; Nature Publishing Group; Kidney International; 86; 3; 9-2014; 506-514
0085-2538
CONICET Digital
CONICET
url http://hdl.handle.net/11336/95594
identifier_str_mv Ilatovskaya, Daria V.; Palygin, Oleg; Chubinskiy Nadezhdin, Vladislav; Negulyaev, Yuri A.; Ma, Rong; et al.; Angiotensin II has acute effects on TRPC6 channels in podocytes of freshly isolated glomeruli; Nature Publishing Group; Kidney International; 86; 3; 9-2014; 506-514
0085-2538
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0085253815303240
info:eu-repo/semantics/altIdentifier/doi/10.1038/ki.2014.71
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Nature Publishing Group
publisher.none.fl_str_mv Nature Publishing Group
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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