Hypercysteinemia promotes atherosclerosis by reducing protein S-nitrosylation.
(2015) In Biomedicine and Pharmacotherapy 70. p.253-259- Abstract
- Protein S-nitrosylation plays important role in the regulation of cardiovascular functions in nitric oxide (NO) Pathway. Hypercysteinemia (HHcy) is an independently risk factor for atherosclerosis. We hypothesized that HHcy promotes atherosclerosis by reducing level of vascular protein S-nitrosylation. The aim of present study is to investigate effect of HHcy on vascular protein S-nitrosylation. A total of 45 male apoE-/- mice were randomly divided into three groups. The control group was fed a Western-type diet. The HHcy group was fed a diet containing 4.4% l-methionine, and the HHcy+NONOate group was fed a diet containing 4.4% l-methionine and administrated NONOate (ip). Human umbilical vein endothelial cells were performed for in vitro... (More)
- Protein S-nitrosylation plays important role in the regulation of cardiovascular functions in nitric oxide (NO) Pathway. Hypercysteinemia (HHcy) is an independently risk factor for atherosclerosis. We hypothesized that HHcy promotes atherosclerosis by reducing level of vascular protein S-nitrosylation. The aim of present study is to investigate effect of HHcy on vascular protein S-nitrosylation. A total of 45 male apoE-/- mice were randomly divided into three groups. The control group was fed a Western-type diet. The HHcy group was fed a diet containing 4.4% l-methionine, and the HHcy+NONOate group was fed a diet containing 4.4% l-methionine and administrated NONOate (ip). Human umbilical vein endothelial cells were performed for in vitro experiment. Plasma lipids were measured every 4 weeks. After 12 weeks, aortic atherosclerotic lesion areas were detected as well as cellular components. The levels of plasma homocysteine (Hcy) and NO were measured. S-nitrosylation was detected using immunofluorescence, and further confirmed by biotin switch method. We found that compared with the control group, Hcy levels, and atherosclerotic plaque, and content of vascular smooth muscle cells and macrophages in lesions significantly increased, and levels of NO significantly decreased in the HHcy group. However, NONOate reverses this effect. In addition, Hcy significantly reduced protein S-nitrosylation in human umbilical vein endothelial cells. This reduction of protein S-nitrosylation was accompanied by reduced levels of NO. Our results suggested that Hcy promoted atherosclerosis by inhibiting vascular protein S-nitrosylation. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/5258505
- author
- Chen, Yulong ; Liu, Ruihan ; Zhang, Guangwei ; Yu, Qi ; Jia, Min ; Zheng, Chao ; Wang, Yanli ; Xu, Cangbao ; Zhang, Yaping LU and Liu, Enqi
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Biomedicine and Pharmacotherapy
- volume
- 70
- pages
- 253 - 259
- publisher
- Elsevier
- external identifiers
-
- pmid:25776509
- wos:000351019300040
- scopus:84927511147
- pmid:25776509
- ISSN
- 1950-6007
- DOI
- 10.1016/j.biopha.2015.01.030
- language
- English
- LU publication?
- yes
- id
- b6a857c7-0492-437f-b819-391335e5d426 (old id 5258505)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/25776509?dopt=Abstract
- date added to LUP
- 2016-04-01 10:46:15
- date last changed
- 2024-02-05 13:15:33
@article{b6a857c7-0492-437f-b819-391335e5d426,
abstract = {{Protein S-nitrosylation plays important role in the regulation of cardiovascular functions in nitric oxide (NO) Pathway. Hypercysteinemia (HHcy) is an independently risk factor for atherosclerosis. We hypothesized that HHcy promotes atherosclerosis by reducing level of vascular protein S-nitrosylation. The aim of present study is to investigate effect of HHcy on vascular protein S-nitrosylation. A total of 45 male apoE-/- mice were randomly divided into three groups. The control group was fed a Western-type diet. The HHcy group was fed a diet containing 4.4% l-methionine, and the HHcy+NONOate group was fed a diet containing 4.4% l-methionine and administrated NONOate (ip). Human umbilical vein endothelial cells were performed for in vitro experiment. Plasma lipids were measured every 4 weeks. After 12 weeks, aortic atherosclerotic lesion areas were detected as well as cellular components. The levels of plasma homocysteine (Hcy) and NO were measured. S-nitrosylation was detected using immunofluorescence, and further confirmed by biotin switch method. We found that compared with the control group, Hcy levels, and atherosclerotic plaque, and content of vascular smooth muscle cells and macrophages in lesions significantly increased, and levels of NO significantly decreased in the HHcy group. However, NONOate reverses this effect. In addition, Hcy significantly reduced protein S-nitrosylation in human umbilical vein endothelial cells. This reduction of protein S-nitrosylation was accompanied by reduced levels of NO. Our results suggested that Hcy promoted atherosclerosis by inhibiting vascular protein S-nitrosylation.}},
author = {{Chen, Yulong and Liu, Ruihan and Zhang, Guangwei and Yu, Qi and Jia, Min and Zheng, Chao and Wang, Yanli and Xu, Cangbao and Zhang, Yaping and Liu, Enqi}},
issn = {{1950-6007}},
language = {{eng}},
pages = {{253--259}},
publisher = {{Elsevier}},
series = {{Biomedicine and Pharmacotherapy}},
title = {{Hypercysteinemia promotes atherosclerosis by reducing protein S-nitrosylation.}},
url = {{http://dx.doi.org/10.1016/j.biopha.2015.01.030}},
doi = {{10.1016/j.biopha.2015.01.030}},
volume = {{70}},
year = {{2015}},
}