LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis

Baoyu Qin,1 Xiaoli Cao2 1Division of Endocrinology and Metabolic, Department of Geriatrics, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi Zhuang Autonomous Region, People’s Republic of China; 2Department of Endocrinology, Shanxi Cardiovascular Hospit...

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Autores principales:	Qin B, Cao X
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2021
Materias:	diabetic nephropathy lncrna pvt1 mir-325-3p snail1 Specialties of internal medicine RC581-951
Acceso en línea:	https://doaj.org/article/24cdcd6074794b6baeb029f5cddb8aca
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spelling	oai:doaj.org-article:24cdcd6074794b6baeb029f5cddb8aca2021-12-02T18:06:47ZLncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis1178-7007https://doaj.org/article/24cdcd6074794b6baeb029f5cddb8aca2021-04-01T00:00:00Zhttps://www.dovepress.com/lncrna-pvt1-regulates-high-glucose-induced-viability-oxidative-stress--peer-reviewed-fulltext-article-DMSOhttps://doaj.org/toc/1178-7007Baoyu Qin,1 Xiaoli Cao2 1Division of Endocrinology and Metabolic, Department of Geriatrics, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi Zhuang Autonomous Region, People’s Republic of China; 2Department of Endocrinology, Shanxi Cardiovascular Hospital, Taiyuan, 030024, Shanxi Province, People’s Republic of ChinaCorrespondence: Baoyu QinDivision of Endocrinology and Metabolic, Department of Geriatrics, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi Zhuang Autonomous Region, People’s Republic of ChinaTel +86-13977179605Email qbaoyu1989@163.comBackground: Diabetic nephropathy (DN), as a complication of diabetes, is a leading cause of mortality in diabetic patients. It has been reported that lncRNA PVT1 (PVT1) could accelerate the progression of DN by promoting ECM accumulation and increasing the expression of fibronectin 1 (FN1). However, the underlying mechanism of PVT1 on DN remains unknown.Methods: To study the effect of PVT1 on DN, mice were injected 50 mg/kg STZ to build the DN models. Mesangial cells (MCs) were induced by high glucose as in vitro model of DN. The expression level of PVT1, miR-325-3 and Snail1 was assessed by qRT-PCR and Western blot. Luciferase reporter assay, RNA pull-down and RIP were used to explore the interaction among PVT1, miR-325-3 and Snail1.Results: In in vivo and in vitro DN models, the expression of PVT1 was upregulated. High glucose (HG) induced cell viability, oxidative stress, fibrosis and inflammation in MCs, which were reversed in the PVT1-KD MCs. The level of miR-325-3p was also increased in in vivo and in vitro experiments. Additionally, PVT1 can directly bind to miR-325-3p. Finally, Snail1 was a direct target of miR-325-3p.Conclusion: PVT1 inhibits viability, oxidative stress, fibrosis, and inflammation in DN via miR-325-3p/Snail1 axis.Keywords: diabetic nephropathy, lncRNA PVT1, miR-325-3p, Snail1Qin BCao XDove Medical Pressarticlediabetic nephropathylncrna pvt1mir-325-3psnail1Specialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol Volume 14, Pp 1741-1750 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	diabetic nephropathy lncrna pvt1 mir-325-3p snail1 Specialties of internal medicine RC581-951
spellingShingle	diabetic nephropathy lncrna pvt1 mir-325-3p snail1 Specialties of internal medicine RC581-951 Qin B Cao X LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis
description	Baoyu Qin,1 Xiaoli Cao2 1Division of Endocrinology and Metabolic, Department of Geriatrics, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi Zhuang Autonomous Region, People’s Republic of China; 2Department of Endocrinology, Shanxi Cardiovascular Hospital, Taiyuan, 030024, Shanxi Province, People’s Republic of ChinaCorrespondence: Baoyu QinDivision of Endocrinology and Metabolic, Department of Geriatrics, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi Zhuang Autonomous Region, People’s Republic of ChinaTel +86-13977179605Email qbaoyu1989@163.comBackground: Diabetic nephropathy (DN), as a complication of diabetes, is a leading cause of mortality in diabetic patients. It has been reported that lncRNA PVT1 (PVT1) could accelerate the progression of DN by promoting ECM accumulation and increasing the expression of fibronectin 1 (FN1). However, the underlying mechanism of PVT1 on DN remains unknown.Methods: To study the effect of PVT1 on DN, mice were injected 50 mg/kg STZ to build the DN models. Mesangial cells (MCs) were induced by high glucose as in vitro model of DN. The expression level of PVT1, miR-325-3 and Snail1 was assessed by qRT-PCR and Western blot. Luciferase reporter assay, RNA pull-down and RIP were used to explore the interaction among PVT1, miR-325-3 and Snail1.Results: In in vivo and in vitro DN models, the expression of PVT1 was upregulated. High glucose (HG) induced cell viability, oxidative stress, fibrosis and inflammation in MCs, which were reversed in the PVT1-KD MCs. The level of miR-325-3p was also increased in in vivo and in vitro experiments. Additionally, PVT1 can directly bind to miR-325-3p. Finally, Snail1 was a direct target of miR-325-3p.Conclusion: PVT1 inhibits viability, oxidative stress, fibrosis, and inflammation in DN via miR-325-3p/Snail1 axis.Keywords: diabetic nephropathy, lncRNA PVT1, miR-325-3p, Snail1
format	article
author	Qin B Cao X
author_facet	Qin B Cao X
author_sort	Qin B
title	LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis
title_short	LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis
title_full	LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis
title_fullStr	LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis
title_full_unstemmed	LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis
title_sort	lncrna pvt1 regulates high glucose-induced viability, oxidative stress, fibrosis, and inflammation in diabetic nephropathy via mir-325-3p/snail1 axis
publisher	Dove Medical Press
publishDate	2021
url	https://doaj.org/article/24cdcd6074794b6baeb029f5cddb8aca
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LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis

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