Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension

Objective: This study aimed to determine the communicational pattern of gaseous signaling molecules sulfur dioxide (SO2) and nitric oxide (NO) between vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs), and elucidate the compensatory role and significance of endogenous SO2 in...

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Autores principales:	Yunjia Song, Jiaru Song, Zhigang Zhu, Hanlin Peng, Xiang Ding, Fuquan Yang, Kun Li, Xiaoqi Yu, Guosheng Yang, Yinghong Tao, Dingfang Bu, Chaoshu Tang, Yaqian Huang, Junbao Du, Hongfang Jin
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Sulfur dioxide Aspartate aminotransferase S-Nitrosylation Endothelial cells Remodeling Medicine (General) R5-920 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/fcb24e0fd2b44b8292ba827a1cdc73a1
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spelling	oai:doaj.org-article:fcb24e0fd2b44b8292ba827a1cdc73a12021-11-24T04:29:10ZCompensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension2213-231710.1016/j.redox.2021.102192https://doaj.org/article/fcb24e0fd2b44b8292ba827a1cdc73a12021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2213231721003529https://doaj.org/toc/2213-2317Objective: This study aimed to determine the communicational pattern of gaseous signaling molecules sulfur dioxide (SO2) and nitric oxide (NO) between vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs), and elucidate the compensatory role and significance of endogenous SO2 in the development of hypertension due to NO deficiency. Approach and results: Blood pressure was monitored by the tail-cuff and implantable physiological signal telemetry in L-nitro-arginine methyl ester (l-NAME)-induced hypertensive mice, and structural alterations of mouse aortic vessels were detected by the elastic fiber staining method. l-NAME-treated mice showed decreased plasma NO levels, increased SO2 levels, vascular remodeling, and increased blood pressure, and application of l-aspartate-β-hydroxamate, which inhibits SO2 production, further aggravated vascular structural remodeling and increased blood pressure. Moreover, in a co-culture system of HAECs and HASMCs, NO from HAECs did not influence aspartate aminotransferase (AAT)1 protein expression but decreased AAT1 activity in HASMCs, thereby resulting in the inhibition of endogenous SO2 production. Furthermore, NO promoted S-nitrosylation of AAT1 protein in HASMCs and purified AAT1 protein. Liquid chromatography with tandem mass spectrometry showed that the Cys192 site of AAT1 purified protein was modified by S-nitrosylation. In contrast, dithiothreitol or C192S mutations in HASMCs blocked NO-induced AAT1 S-nitrosylation and restored AAT1 enzyme activity. Conclusion: Endothelium-derived NO inhibits AAT activity by nitrosylating AAT1 at the Cys192 site and reduces SO2 production in HASMCs. Our findings suggest that SO2 acts as a compensatory defense system to antagonize vascular structural remodeling and hypertension when the endogenous NO pathway is disturbed.Yunjia SongJiaru SongZhigang ZhuHanlin PengXiang DingFuquan YangKun LiXiaoqi YuGuosheng YangYinghong TaoDingfang BuChaoshu TangYaqian HuangJunbao DuHongfang JinElsevierarticleSulfur dioxideAspartate aminotransferaseS-NitrosylationEndothelial cellsRemodelingMedicine (General)R5-920Biology (General)QH301-705.5ENRedox Biology, Vol 48, Iss , Pp 102192- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Sulfur dioxide Aspartate aminotransferase S-Nitrosylation Endothelial cells Remodeling Medicine (General) R5-920 Biology (General) QH301-705.5
spellingShingle	Sulfur dioxide Aspartate aminotransferase S-Nitrosylation Endothelial cells Remodeling Medicine (General) R5-920 Biology (General) QH301-705.5 Yunjia Song Jiaru Song Zhigang Zhu Hanlin Peng Xiang Ding Fuquan Yang Kun Li Xiaoqi Yu Guosheng Yang Yinghong Tao Dingfang Bu Chaoshu Tang Yaqian Huang Junbao Du Hongfang Jin Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension
description	Objective: This study aimed to determine the communicational pattern of gaseous signaling molecules sulfur dioxide (SO2) and nitric oxide (NO) between vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs), and elucidate the compensatory role and significance of endogenous SO2 in the development of hypertension due to NO deficiency. Approach and results: Blood pressure was monitored by the tail-cuff and implantable physiological signal telemetry in L-nitro-arginine methyl ester (l-NAME)-induced hypertensive mice, and structural alterations of mouse aortic vessels were detected by the elastic fiber staining method. l-NAME-treated mice showed decreased plasma NO levels, increased SO2 levels, vascular remodeling, and increased blood pressure, and application of l-aspartate-β-hydroxamate, which inhibits SO2 production, further aggravated vascular structural remodeling and increased blood pressure. Moreover, in a co-culture system of HAECs and HASMCs, NO from HAECs did not influence aspartate aminotransferase (AAT)1 protein expression but decreased AAT1 activity in HASMCs, thereby resulting in the inhibition of endogenous SO2 production. Furthermore, NO promoted S-nitrosylation of AAT1 protein in HASMCs and purified AAT1 protein. Liquid chromatography with tandem mass spectrometry showed that the Cys192 site of AAT1 purified protein was modified by S-nitrosylation. In contrast, dithiothreitol or C192S mutations in HASMCs blocked NO-induced AAT1 S-nitrosylation and restored AAT1 enzyme activity. Conclusion: Endothelium-derived NO inhibits AAT activity by nitrosylating AAT1 at the Cys192 site and reduces SO2 production in HASMCs. Our findings suggest that SO2 acts as a compensatory defense system to antagonize vascular structural remodeling and hypertension when the endogenous NO pathway is disturbed.
format	article
author	Yunjia Song Jiaru Song Zhigang Zhu Hanlin Peng Xiang Ding Fuquan Yang Kun Li Xiaoqi Yu Guosheng Yang Yinghong Tao Dingfang Bu Chaoshu Tang Yaqian Huang Junbao Du Hongfang Jin
author_facet	Yunjia Song Jiaru Song Zhigang Zhu Hanlin Peng Xiang Ding Fuquan Yang Kun Li Xiaoqi Yu Guosheng Yang Yinghong Tao Dingfang Bu Chaoshu Tang Yaqian Huang Junbao Du Hongfang Jin
author_sort	Yunjia Song
title	Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension
title_short	Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension
title_full	Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension
title_fullStr	Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension
title_full_unstemmed	Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension
title_sort	compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/fcb24e0fd2b44b8292ba827a1cdc73a1
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Compensatory role of endogenous sulfur dioxide in nitric oxide deficiency-induced hypertension

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