MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration

Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) and excessive accumulation of dysfunctional PVAT are hallmarks of pathogenesis after angioplasty. Recent genome-wide association studies reveal that single-nucleotide polymorphism (SNP) in MIA3 is associated with atheroscle...

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Autores principales:	Yu Lei, Jianfei Xu, Mengju Li, Ting Meng, Meihua Chen, Yongfeng Yang, Hongda Li, Tao Zhuang, Junli Zuo
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	PVAT MIA3 VSMCs neointima adipocytes Diseases of the endocrine glands. Clinical endocrinology RC648-665
Acceso en línea:	https://doaj.org/article/fbe676ff8a85442fa42d7da8770c953e
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spelling	oai:doaj.org-article:fbe676ff8a85442fa42d7da8770c953e2021-11-10T11:59:17ZMIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration1664-239210.3389/fendo.2021.748216https://doaj.org/article/fbe676ff8a85442fa42d7da8770c953e2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fendo.2021.748216/fullhttps://doaj.org/toc/1664-2392Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) and excessive accumulation of dysfunctional PVAT are hallmarks of pathogenesis after angioplasty. Recent genome-wide association studies reveal that single-nucleotide polymorphism (SNP) in MIA3 is associated with atherosclerosis-relevant VSMC phenotypes. However, the role of MIA3 in the vascular remodeling response to injury remains unknown. Here, we found that expression of MIA3 is increased in proliferative VSMCs and knockdown of MIA3 reduces VSMCs proliferation, migration, and inflammation, whereas MIA3 overexpression promoted VSMC migration and proliferation. Moreover, knockdown of MIA3 ameliorates femoral artery wire injury-induced neointimal hyperplasia and increases brown-like perivascular adipocytes. Collectively, the data suggest that MIA3 deficiency prevents neointimal formation by decreasing VSMC proliferation, migration, and inflammation and maintaining BAT-like perivascular adipocytes in PVAT during injury-induced vascular remodeling, which provide a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases.Yu LeiYu LeiYu LeiJianfei XuMengju LiTing MengMeihua ChenYongfeng YangHongda LiTao ZhuangTao ZhuangJunli ZuoFrontiers Media S.A.articlePVATMIA3VSMCsneointimaadipocytesDiseases of the endocrine glands. Clinical endocrinologyRC648-665ENFrontiers in Endocrinology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	PVAT MIA3 VSMCs neointima adipocytes Diseases of the endocrine glands. Clinical endocrinology RC648-665
spellingShingle	PVAT MIA3 VSMCs neointima adipocytes Diseases of the endocrine glands. Clinical endocrinology RC648-665 Yu Lei Yu Lei Yu Lei Jianfei Xu Mengju Li Ting Meng Meihua Chen Yongfeng Yang Hongda Li Tao Zhuang Tao Zhuang Junli Zuo MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration
description	Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) and excessive accumulation of dysfunctional PVAT are hallmarks of pathogenesis after angioplasty. Recent genome-wide association studies reveal that single-nucleotide polymorphism (SNP) in MIA3 is associated with atherosclerosis-relevant VSMC phenotypes. However, the role of MIA3 in the vascular remodeling response to injury remains unknown. Here, we found that expression of MIA3 is increased in proliferative VSMCs and knockdown of MIA3 reduces VSMCs proliferation, migration, and inflammation, whereas MIA3 overexpression promoted VSMC migration and proliferation. Moreover, knockdown of MIA3 ameliorates femoral artery wire injury-induced neointimal hyperplasia and increases brown-like perivascular adipocytes. Collectively, the data suggest that MIA3 deficiency prevents neointimal formation by decreasing VSMC proliferation, migration, and inflammation and maintaining BAT-like perivascular adipocytes in PVAT during injury-induced vascular remodeling, which provide a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases.
format	article
author	Yu Lei Yu Lei Yu Lei Jianfei Xu Mengju Li Ting Meng Meihua Chen Yongfeng Yang Hongda Li Tao Zhuang Tao Zhuang Junli Zuo
author_facet	Yu Lei Yu Lei Yu Lei Jianfei Xu Mengju Li Ting Meng Meihua Chen Yongfeng Yang Hongda Li Tao Zhuang Tao Zhuang Junli Zuo
author_sort	Yu Lei
title	MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration
title_short	MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration
title_full	MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration
title_fullStr	MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration
title_full_unstemmed	MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration
title_sort	mia sh3 domain er export factor 3 deficiency prevents neointimal formation by restoring bat-like pvat and decreasing vsmc proliferation and migration
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/fbe676ff8a85442fa42d7da8770c953e
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MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration

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