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Hypercysteinemia promotes atherosclerosis by reducing protein S-nitrosylation
Yulong Chen1, Ruihan Liu2, Guangwei Zhang3
1Shaanxi Key Laboratory of Ischemic Cardiovascular Disease, Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an, Shaanxi 710021, China; Laboratory Animal Center, Xi'an Jiaotong University School of Medicine, Xi'an Shaanxi, 710061, China.
Summary
Hyperhomocysteinemia (HHcy) promotes atherosclerosis by reducing vascular protein S-nitrosylation. Supplementation with NONOate reversed these effects, indicating a potential therapeutic target for cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Biochemistry
- Pathophysiology
Background:
- Protein S-nitrosylation is crucial for cardiovascular function within the nitric oxide (NO) pathway.
- Hyperhomocysteinemia (HHcy) is an established risk factor for atherosclerosis.
- The precise mechanism by which HHcy influences vascular S-nitrosylation remains unclear.
Purpose of the Study:
- To investigate the effect of HHcy on vascular protein S-nitrosylation.
- To determine if HHcy promotes atherosclerosis by reducing S-nitrosylation levels.
- To explore the potential of NO supplementation to counteract HHcy-induced effects.
Main Methods:
- ApoE-/- mice were divided into control, HHcy, and HHcy+NONOate groups, fed specific diets for 12 weeks.
- In vitro studies used human umbilical vein endothelial cells exposed to homocysteine (Hcy).
- Measurements included plasma lipids, homocysteine, NO, atherosclerotic lesion area, and protein S-nitrosylation via immunofluorescence and biotin switch assay.
Main Results:
- HHcy significantly increased Hcy levels, atherosclerotic plaque area, and infiltration of vascular smooth muscle cells and macrophages.
- HHcy led to decreased NO levels and reduced vascular protein S-nitrosylation.
- NONOate administration reversed the detrimental effects of HHcy, while in vitro Hcy reduced S-nitrosylation in endothelial cells.
Conclusions:
- HHcy promotes atherosclerosis by inhibiting vascular protein S-nitrosylation.
- Reduced NO bioavailability is linked to decreased S-nitrosylation in HHcy.
- Targeting S-nitrosylation pathways may offer a therapeutic strategy against HHcy-driven atherosclerosis.
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