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Hypercysteinemia promotes atherosclerosis by reducing protein S-nitrosylation.

Chen, Yulong; Liu, Ruihan; Zhang, Guangwei; Yu, Qi; Jia, Min; Zheng, Chao; Wang, Yanli; Xu, Cangbao; Zhang, Yaping LU and Liu, Enqi (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)
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organization
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type
Contribution to journal
publication status
published
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in
Biomedicine and Pharmacotherapy
volume
70
pages
253 - 259
publisher
Elsevier
external identifiers
  • pmid:25776509
  • wos:000351019300040
  • scopus:84927511147
ISSN
1950-6007
DOI
10.1016/j.biopha.2015.01.030
language
English
LU publication?
yes
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b6a857c7-0492-437f-b819-391335e5d426 (old id 5258505)
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http://www.ncbi.nlm.nih.gov/pubmed/25776509?dopt=Abstract
date added to LUP
2015-04-03 21:06:09
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2017-10-01 03:22:52
@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},
  volume       = {70},
  year         = {2015},
}