FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p

Abstract The proliferation and migration of vascular smooth muscle cells (VSMCs) play an essential role during the development of cardiovascular diseases (CVDs). While many factors potentially contribute to the abnormal activation of VSMCs, hyperglycemia is generally believed to be a major causative...

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Autores principales:	Wenxiang Zhang, Siyu Chen, Zhao Zhang, Chen Wang, Chang Liu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ed4db819272140649fa1ec157637c204
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spelling	oai:doaj.org-article:ed4db819272140649fa1ec157637c2042021-12-02T16:06:07ZFAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p10.1038/s41598-017-02683-32045-2322https://doaj.org/article/ed4db819272140649fa1ec157637c2042017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02683-3https://doaj.org/toc/2045-2322Abstract The proliferation and migration of vascular smooth muscle cells (VSMCs) play an essential role during the development of cardiovascular diseases (CVDs). While many factors potentially contribute to the abnormal activation of VSMCs, hyperglycemia is generally believed to be a major causative factor. On the other hand, FAM3B (named PANDER for its secretory form) is a uniquely structured protein strongly expressed within and secreted from the endocrine pancreas. FAM3B is co-secreted with insulin from the β-cell upon glucose stimulation and regulates glucose homeostasis. In the present study, we sought to determine the roles of FAM3B in the regulation of VSMC physiology, especially under the hyperglycemic condition. We found that FAM3B expression was induced by hyperglycemia both in vivo and in vitro. FAM3B knockdown inhibited, whereas FAM3B overexpression accelerated VSMC proliferation and migration. At the molecular level, FAM3B inhibited miR-322-5p expression, and enforced expression of miR-322-5p antagonized FAM3B-induced VSMC proliferation and migration, suggesting that FAM3B facilitated VSMC pathological activation via miR-322-5p. Taken together, FAM3B mediates high glucose-induced VSMC proliferation and migration via inhibition of miR-322-5p. Thus, FAM3B may therefore serve as a novel therapeutic target for diabetes-related CVDs.Wenxiang ZhangSiyu ChenZhao ZhangChen WangChang LiuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Wenxiang Zhang Siyu Chen Zhao Zhang Chen Wang Chang Liu FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p
description	Abstract The proliferation and migration of vascular smooth muscle cells (VSMCs) play an essential role during the development of cardiovascular diseases (CVDs). While many factors potentially contribute to the abnormal activation of VSMCs, hyperglycemia is generally believed to be a major causative factor. On the other hand, FAM3B (named PANDER for its secretory form) is a uniquely structured protein strongly expressed within and secreted from the endocrine pancreas. FAM3B is co-secreted with insulin from the β-cell upon glucose stimulation and regulates glucose homeostasis. In the present study, we sought to determine the roles of FAM3B in the regulation of VSMC physiology, especially under the hyperglycemic condition. We found that FAM3B expression was induced by hyperglycemia both in vivo and in vitro. FAM3B knockdown inhibited, whereas FAM3B overexpression accelerated VSMC proliferation and migration. At the molecular level, FAM3B inhibited miR-322-5p expression, and enforced expression of miR-322-5p antagonized FAM3B-induced VSMC proliferation and migration, suggesting that FAM3B facilitated VSMC pathological activation via miR-322-5p. Taken together, FAM3B mediates high glucose-induced VSMC proliferation and migration via inhibition of miR-322-5p. Thus, FAM3B may therefore serve as a novel therapeutic target for diabetes-related CVDs.
format	article
author	Wenxiang Zhang Siyu Chen Zhao Zhang Chen Wang Chang Liu
author_facet	Wenxiang Zhang Siyu Chen Zhao Zhang Chen Wang Chang Liu
author_sort	Wenxiang Zhang
title	FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p
title_short	FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p
title_full	FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p
title_fullStr	FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p
title_full_unstemmed	FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p
title_sort	fam3b mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of mir-322-5p
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/ed4db819272140649fa1ec157637c204
work_keys_str_mv	AT wenxiangzhang fam3bmediateshighglucoseinducedvascularsmoothmusclecellproliferationandmigrationviainhibitionofmir3225p AT siyuchen fam3bmediateshighglucoseinducedvascularsmoothmusclecellproliferationandmigrationviainhibitionofmir3225p AT zhaozhang fam3bmediateshighglucoseinducedvascularsmoothmusclecellproliferationandmigrationviainhibitionofmir3225p AT chenwang fam3bmediateshighglucoseinducedvascularsmoothmusclecellproliferationandmigrationviainhibitionofmir3225p AT changliu fam3bmediateshighglucoseinducedvascularsmoothmusclecellproliferationandmigrationviainhibitionofmir3225p
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FAM3B mediates high glucose-induced vascular smooth muscle cell proliferation and migration via inhibition of miR-322-5p

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