TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction

Abstract p16 inhibits cyclin-dependent kinases and regulates senescence-mediated arrest as well as p21. Nuclear p16 promotes G1 cell cycle arrest and cellular senescence. In various glomerular diseases, nuclear p16 expression is associated with disease progression. Therefore, the location of p16 is...

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Autores principales:	Sayo Ueda, Tatsuya Tominaga, Arisa Ochi, Akiko Sakurai, Kenji Nishimura, Eriko Shibata, Shu Wakino, Masanori Tamaki, Kojiro Nagai
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/91a4759a73d646a09a3b309417eee090
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spelling	oai:doaj.org-article:91a4759a73d646a09a3b309417eee0902021-11-08T10:46:33ZTGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction10.1038/s41598-021-01150-42045-2322https://doaj.org/article/91a4759a73d646a09a3b309417eee0902021-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-01150-4https://doaj.org/toc/2045-2322Abstract p16 inhibits cyclin-dependent kinases and regulates senescence-mediated arrest as well as p21. Nuclear p16 promotes G1 cell cycle arrest and cellular senescence. In various glomerular diseases, nuclear p16 expression is associated with disease progression. Therefore, the location of p16 is important. However, the mechanism of p16 trafficking between the nucleus and cytoplasm is yet to be fully investigated. TGF-β1, a major cytokine involved in the development of kidney diseases, can upregulate p21 expression. However, the relationship between TGF-β1 and p16 is poorly understood. Here, we report the role of podocyte TGF-β1 in regulating the p16 behavior in glomerular endothelial cells. We analyzed podocyte-specific TGF-β1 overexpression mice. Although p16 was found in the nuclei of glomerular endothelial cells and led to endothelial cellular senescence, the expression of p16 did not increase in glomeruli. In cultured endothelial cells, TGF-β1 induced nuclear translocation of p16 without increasing its expression. Among human glomerular diseases, p16 was detected in the nuclei of glomerular endothelial cells. In summary, we demonstrated the novel role of podocyte TGF-β1 in managing p16 behavior and cellular senescence in glomeruli, which has clinical relevance for the progression of human glomerular diseases.Sayo UedaTatsuya TominagaArisa OchiAkiko SakuraiKenji NishimuraEriko ShibataShu WakinoMasanori TamakiKojiro NagaiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sayo Ueda Tatsuya Tominaga Arisa Ochi Akiko Sakurai Kenji Nishimura Eriko Shibata Shu Wakino Masanori Tamaki Kojiro Nagai TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction
description	Abstract p16 inhibits cyclin-dependent kinases and regulates senescence-mediated arrest as well as p21. Nuclear p16 promotes G1 cell cycle arrest and cellular senescence. In various glomerular diseases, nuclear p16 expression is associated with disease progression. Therefore, the location of p16 is important. However, the mechanism of p16 trafficking between the nucleus and cytoplasm is yet to be fully investigated. TGF-β1, a major cytokine involved in the development of kidney diseases, can upregulate p21 expression. However, the relationship between TGF-β1 and p16 is poorly understood. Here, we report the role of podocyte TGF-β1 in regulating the p16 behavior in glomerular endothelial cells. We analyzed podocyte-specific TGF-β1 overexpression mice. Although p16 was found in the nuclei of glomerular endothelial cells and led to endothelial cellular senescence, the expression of p16 did not increase in glomeruli. In cultured endothelial cells, TGF-β1 induced nuclear translocation of p16 without increasing its expression. Among human glomerular diseases, p16 was detected in the nuclei of glomerular endothelial cells. In summary, we demonstrated the novel role of podocyte TGF-β1 in managing p16 behavior and cellular senescence in glomeruli, which has clinical relevance for the progression of human glomerular diseases.
format	article
author	Sayo Ueda Tatsuya Tominaga Arisa Ochi Akiko Sakurai Kenji Nishimura Eriko Shibata Shu Wakino Masanori Tamaki Kojiro Nagai
author_facet	Sayo Ueda Tatsuya Tominaga Arisa Ochi Akiko Sakurai Kenji Nishimura Eriko Shibata Shu Wakino Masanori Tamaki Kojiro Nagai
author_sort	Sayo Ueda
title	TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction
title_short	TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction
title_full	TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction
title_fullStr	TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction
title_full_unstemmed	TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction
title_sort	tgf-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/91a4759a73d646a09a3b309417eee090
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TGF-β1 is involved in senescence-related pathways in glomerular endothelial cells via p16 translocation and p21 induction

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