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Published on: September 7, 2017

Folate and ApoE DNA methylation induced by homocysteine in human monocytes

Jiang Yi-Deng1, Sun Tao, Zhang Hui-Ping

  • 1Department of Pathophysiology, Ning Xia Medical College, Yin Chuan, China. jwcjyd@163.com

DNA and Cell Biology
|September 4, 2007
PubMed

Insights

High homocysteine (Hcy) levels increase cholesterol and decrease apolipoprotein E (ApoE) expression by accelerating ApoE DNA methylation. Folate counteracts these effects, suggesting a therapeutic role in preventing Hcy-induced atherosclerosis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Homocysteine (Hcy) is an independent risk factor for arteriosclerosis.
  • Apolipoprotein E (ApoE) is crucial in anti-atherosclerosis mechanisms.
  • The interplay between Hcy, folate, and ApoE in atherosclerosis pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the impact of Hcy and folate on ApoE expression in monocytes.
  • To elucidate the mechanism by which Hcy induces ApoE expression changes.
  • To assess the potential of folate as a therapeutic agent against Hcy-induced atherosclerosis.

Main Methods:

  • Cultured primary human monocytes treated with clinically relevant concentrations of Hcy and folate.
  • Quantification of total cholesterol (TC), free cholesterol (FC), and cholesteryl ester (CE) levels.
  • Measurement of ApoE mRNA and protein expression.
  • Assessment of C-5 methyltransferase (C-5 MTase) activity and DNA methylation of ApoE.

Main Results:

  • Hcy significantly increased TC, FC, and CE levels.
  • Hcy markedly decreased ApoE mRNA and protein expression (34.28% and 45.00% reduction, respectively).
  • Hcy upregulated C-5 MTase activity, accelerating ApoE DNA methylation.
  • Folate reversed the effects of Hcy, decreasing cholesterol levels and increasing ApoE expression by repressing DNA methylation.

Conclusions:

  • Hcy-induced ApoE DNA methylation plays a role in atherosclerosis development.
  • Folate exhibits beneficial anti-atherosclerotic effects by mitigating Hcy-induced DNA methylation.
  • Folate represents a potential therapeutic target for preventing Hcy-associated atherosclerosis.

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