Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs

Endosulfan is an organochlorine pesticide, which poses a potential danger to human health and safety. It is known that dysfunction of glomerular mesangial cells causes glomerular sclerosis, associated with chronic kidney diseases. In the present study, we investigated the effects of endosulfan on ce...

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Autores principales:	Shiwen Liu, Yumeng Hu, Yue Wang, Yeqing Sun, Shu-Lan Qin, Dan Xu
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Endosulfan Cell proliferation ECM accumulation TGF-β signaling pathway HRMCs Environmental pollution TD172-193.5 Environmental sciences GE1-350
Acceso en línea:	https://doaj.org/article/bb11ce82bb454190817cc9d1cfe26b3b
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spelling	oai:doaj.org-article:bb11ce82bb454190817cc9d1cfe26b3b2021-12-02T04:58:57ZEndosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs0147-651310.1016/j.ecoenv.2021.113040https://doaj.org/article/bb11ce82bb454190817cc9d1cfe26b3b2021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321011520https://doaj.org/toc/0147-6513Endosulfan is an organochlorine pesticide, which poses a potential danger to human health and safety. It is known that dysfunction of glomerular mesangial cells causes glomerular sclerosis, associated with chronic kidney diseases. In the present study, we investigated the effects of endosulfan on cell proliferation and extracellular matrix accumulation (ECM) in human renal mesangial cells (HRMCs). Cells were treated with endosulfan, endosulfan (10 μM) plus specific inhibitor of TGF-β signaling (LY2109761) or antioxidant (NAC). The results showed that endosulfan significantly promoted cell proliferation, accompanied with the decrease of p27 mRNA expression and the increase in the mRNA expression levels of p21 and inflammatory factors IL-6/IL-8. qRT-PCR results showed that matrix metalloproteinase-2 (MMP2) and tissue metalloproteinase-3 (TIMP3) were down-regulated whereas laminin was up-regulated when exposure to endosulfan. Western blot results showed that p-Smad2/3 was up-regulated, while Smad7 was down-regulated when exposure to endosulfan, which were reversed in the presence of LY2109761. Endosulfan significantly decreased the activity of SOD and increased the MDA level and CAT activity, which were reversed in the presence of NAC. These findings suggest that endosulfan can cause excessive proliferation and massive accumulation of ECM through TGF-β/Smad signaling pathway, and also induced oxidative stress and inflammation in HRMCs.Shiwen LiuYumeng HuYue WangYeqing SunShu-Lan QinDan XuElsevierarticleEndosulfanCell proliferationECM accumulationTGF-β signaling pathwayHRMCsEnvironmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 228, Iss , Pp 113040- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Endosulfan Cell proliferation ECM accumulation TGF-β signaling pathway HRMCs Environmental pollution TD172-193.5 Environmental sciences GE1-350
spellingShingle	Endosulfan Cell proliferation ECM accumulation TGF-β signaling pathway HRMCs Environmental pollution TD172-193.5 Environmental sciences GE1-350 Shiwen Liu Yumeng Hu Yue Wang Yeqing Sun Shu-Lan Qin Dan Xu Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs
description	Endosulfan is an organochlorine pesticide, which poses a potential danger to human health and safety. It is known that dysfunction of glomerular mesangial cells causes glomerular sclerosis, associated with chronic kidney diseases. In the present study, we investigated the effects of endosulfan on cell proliferation and extracellular matrix accumulation (ECM) in human renal mesangial cells (HRMCs). Cells were treated with endosulfan, endosulfan (10 μM) plus specific inhibitor of TGF-β signaling (LY2109761) or antioxidant (NAC). The results showed that endosulfan significantly promoted cell proliferation, accompanied with the decrease of p27 mRNA expression and the increase in the mRNA expression levels of p21 and inflammatory factors IL-6/IL-8. qRT-PCR results showed that matrix metalloproteinase-2 (MMP2) and tissue metalloproteinase-3 (TIMP3) were down-regulated whereas laminin was up-regulated when exposure to endosulfan. Western blot results showed that p-Smad2/3 was up-regulated, while Smad7 was down-regulated when exposure to endosulfan, which were reversed in the presence of LY2109761. Endosulfan significantly decreased the activity of SOD and increased the MDA level and CAT activity, which were reversed in the presence of NAC. These findings suggest that endosulfan can cause excessive proliferation and massive accumulation of ECM through TGF-β/Smad signaling pathway, and also induced oxidative stress and inflammation in HRMCs.
format	article
author	Shiwen Liu Yumeng Hu Yue Wang Yeqing Sun Shu-Lan Qin Dan Xu
author_facet	Shiwen Liu Yumeng Hu Yue Wang Yeqing Sun Shu-Lan Qin Dan Xu
author_sort	Shiwen Liu
title	Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs
title_short	Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs
title_full	Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs
title_fullStr	Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs
title_full_unstemmed	Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs
title_sort	endosulfan promotes cell proliferation and extracellular matrix accumulation through tgf-β/smad signaling pathway in hrmcs
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/bb11ce82bb454190817cc9d1cfe26b3b
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Endosulfan promotes cell proliferation and extracellular matrix accumulation through TGF-β/Smad signaling pathway in HRMCs

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