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Cardiovascular Research 2001 52(2):328-336; doi:10.1016/S0008-6363(01)00376-5
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Effects of homocysteine on murine splenic B lymphocyte proliferation and its signal transduction mechanism

Qin Zhanga, Xiaokun Zenga, Jingxuan Guoa and Xian Wanga,b,*

aInstitute of Vascular Medicine, Third Hospital, Beijing 100083, People's Republic of China
bDepartment of Physiology, Health Science Center, Peking University, No. 38, Xue Yuan Road, Beijing 100083, People's Republic of China

* Corresponding author. Tel.: +86-10-6209-1443; fax: +86-10-6201-7700 xwang{at}mail.bjmu.edu.cn

Objective: Elevated plasma homocysteine (Hcy) levels have been defined as an increased risk of atherosclerosis. However, the mechanisms that Hcy induces the development of atherosclerosis are not fully understood. Therefore, effect of Hcy on B lymphocyte proliferation and its cellular mechanism were examined in normal and hyperhomocysteinemia ApoE-knockout mice. Methods: Mouse B lymphocytes were incubated with Hcy, related compounds and/or antioxidants and/or inhibitors of PKC, p38 MAPK, NF-{kappa}B in the presence or absence of lipopolysaccharide. DNA synthesis, production of reactive oxygen species was measured. Results: Hcy (0.1–3.0 mM) and other compounds with thiol (–SH), such as cysteine and glutathione significantly increased resting and lipopolysaccharide-induced B lymphocyte proliferation. ApoE-knockout mice with hypercysteinemia (plasma Hcy levels were 20.3±2.9 vs. 2.6±0.6 µM in control, P<0.05) had a significant promotion of B cell proliferation in response to lipopolysaccharide. Hcy also increased intracellular reactive oxygen species production. Radical scavengers reduced Hcy-induced B lymphocyte proliferation. The promotion of Hcy was significantly inhibited by inhibitors of PKC (calphostin C and RO-31-8220), p38 MAPK (SB 202190 and PD 169316) and NF-{kappa}B (pyrrolidine dithiocarbamate). Conclusions: The reactive oxygen species generated by thiol (–SH) auto-oxidation of Hcy are essential, and PKC, p38 MAPK and NF-{kappa}B are involved in the Hcy-induced B lymphocyte proliferation. Hyperhomocysteinemia may increase B lymphocyte susceptibility to inflammatory progression of atherosclerotic lesions.

KEYWORDS Atherosclerosis; Free radicals; Immunology; Infection/inflammation; Signal transduction


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J. Feng, Z. Zhang, W. Kong, B. Liu, Q. Xu, and X. Wang
Regulatory T cells ameliorate hyperhomocysteinaemia-accelerated atherosclerosis in apoE-/- mice
Cardiovasc Res, July 1, 2009; (2009) cvp182v2.
[Abstract] [Full Text] [PDF]


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