Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs

Vascular hyporesponsiveness in the shock decompensation period is an important factor leading to death. Myosin light chain 20 (MLC20) is the main effector protein that regulates vascular reactivity. However, whether the change in semicarbazide-sensitive amine oxidase (SSAO) expression during hypoxia...

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Autores principales:	Zhang Yuxing, Zhang Xiliang, Cao Zhen, Huang Yun, Zheng Yuexin, Yang Xiaodong
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	ssao mlc20 inos vascular hyporesponsiveness Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/50073839f4654031883e4fecd4584730
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spelling	oai:doaj.org-article:50073839f4654031883e4fecd45847302021-12-05T14:10:42ZEndothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs2391-541210.1515/biol-2021-0114https://doaj.org/article/50073839f4654031883e4fecd45847302021-10-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0114https://doaj.org/toc/2391-5412Vascular hyporesponsiveness in the shock decompensation period is an important factor leading to death. Myosin light chain 20 (MLC20) is the main effector protein that regulates vascular reactivity. However, whether the change in semicarbazide-sensitive amine oxidase (SSAO) expression during hypoxia can change the MLC20 phosphorylation level, and its underlying mechanism were not clear. The amine oxidase copper containing 3 (AOC3) overexpressing adenovirus vector was constructed and transfected into rat intestinal microvascular endothelial cells (RIMECs) to overexpress SSAO, and the RIMECs were co-cultured with rat intestinal microvascular smooth muscle cells (RIMSCs). The changes in SSAO/inducible nitric oxide synthase (iNOS)/Rho associate coiled-coil containing protein kinase 1 (ROCK1) expression levels and MLC20 phosphorylation level were detected. Here we found that the increased SSAO by AOC3 overexpression can decrease the iNOS expression level and its activity after hypoxia. In addition, RIMSCs co-cultured with RIMECs overexpressed with AOC3 gene had significantly higher ROCK1 protein level and MLC20 phosphorylation level than RIMSCs co-cultured with normal RIMECs. Our study demonstrated that SSAO overexpression can significantly inhibit iNOS activity, promote RhoA/ROCK pathway activation, and increase the phosphorylation level of MLC20, which might be the potential mechanism in relieving the vascular hyporesponsiveness during shock decompensation.Zhang YuxingZhang XiliangCao ZhenHuang YunZheng YuexinYang XiaodongDe Gruyterarticlessaomlc20 inosvascular hyporesponsivenessBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 1141-1150 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	ssao mlc20 inos vascular hyporesponsiveness Biology (General) QH301-705.5
spellingShingle	ssao mlc20 inos vascular hyporesponsiveness Biology (General) QH301-705.5 Zhang Yuxing Zhang Xiliang Cao Zhen Huang Yun Zheng Yuexin Yang Xiaodong Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs
description	Vascular hyporesponsiveness in the shock decompensation period is an important factor leading to death. Myosin light chain 20 (MLC20) is the main effector protein that regulates vascular reactivity. However, whether the change in semicarbazide-sensitive amine oxidase (SSAO) expression during hypoxia can change the MLC20 phosphorylation level, and its underlying mechanism were not clear. The amine oxidase copper containing 3 (AOC3) overexpressing adenovirus vector was constructed and transfected into rat intestinal microvascular endothelial cells (RIMECs) to overexpress SSAO, and the RIMECs were co-cultured with rat intestinal microvascular smooth muscle cells (RIMSCs). The changes in SSAO/inducible nitric oxide synthase (iNOS)/Rho associate coiled-coil containing protein kinase 1 (ROCK1) expression levels and MLC20 phosphorylation level were detected. Here we found that the increased SSAO by AOC3 overexpression can decrease the iNOS expression level and its activity after hypoxia. In addition, RIMSCs co-cultured with RIMECs overexpressed with AOC3 gene had significantly higher ROCK1 protein level and MLC20 phosphorylation level than RIMSCs co-cultured with normal RIMECs. Our study demonstrated that SSAO overexpression can significantly inhibit iNOS activity, promote RhoA/ROCK pathway activation, and increase the phosphorylation level of MLC20, which might be the potential mechanism in relieving the vascular hyporesponsiveness during shock decompensation.
format	article
author	Zhang Yuxing Zhang Xiliang Cao Zhen Huang Yun Zheng Yuexin Yang Xiaodong
author_facet	Zhang Yuxing Zhang Xiliang Cao Zhen Huang Yun Zheng Yuexin Yang Xiaodong
author_sort	Zhang Yuxing
title	Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs
title_short	Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs
title_full	Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs
title_fullStr	Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs
title_full_unstemmed	Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs
title_sort	endothelial cell-derived ssao can increase mlc20 phosphorylation in vsmcs
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/50073839f4654031883e4fecd4584730
work_keys_str_mv	AT zhangyuxing endothelialcellderivedssaocanincreasemlc20phosphorylationinvsmcs AT zhangxiliang endothelialcellderivedssaocanincreasemlc20phosphorylationinvsmcs AT caozhen endothelialcellderivedssaocanincreasemlc20phosphorylationinvsmcs AT huangyun endothelialcellderivedssaocanincreasemlc20phosphorylationinvsmcs AT zhengyuexin endothelialcellderivedssaocanincreasemlc20phosphorylationinvsmcs AT yangxiaodong endothelialcellderivedssaocanincreasemlc20phosphorylationinvsmcs
_version_	1718371785419784192

Endothelial cell-derived SSAO can increase MLC20 phosphorylation in VSMCs

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