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Hyperhomocysteinemia promotes inflammatory monocyte generation and accelerates atherosclerosis in transgenic

Daqing Zhang1, Xiaohua Jiang, Pu Fang

  • 1Department of Pharmacology and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA.

Circulation
|October 28, 2009
PubMed

Insights

Hyperhomocysteinemia (HHcy) drives atherosclerosis by increasing inflammatory monocyte subsets. This occurs through NAD(P)H oxidase-mediated oxidative stress, promoting monocyte accumulation in lesions.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Metabolic Disease Research

Background:

  • Hyperhomocysteinemia (HHcy) is a known risk factor for cardiovascular disease.
  • Monocytes, key immune cells, have distinct subsets involved in atherogenesis.
  • This study investigated how HHcy influences monocyte heterogeneity and contributes to atherosclerosis.

Purpose of the Study:

  • To determine if HHcy modulates monocyte heterogeneity.
  • To investigate the role of HHcy in promoting atherosclerosis.
  • To elucidate the mechanisms by which HHcy affects monocyte subsets.

Main Methods:

  • Developed a novel mouse model (Tg-hCBS apoE(-/-) Cbs(-/-)) with severe HHcy and hypercholesterolemia.
  • Utilized a second HHcy mouse model (Tg-S466L Cbs(-/-)) lacking hyperlipidemia.
  • Analyzed monocyte populations and subsets in blood, spleen, and bone marrow.
  • Performed in vitro experiments with l-homocysteine and oxidative stress inhibitors.

Main Results:

  • Severe HHcy accelerated atherosclerosis and inflammatory monocyte/macrophage accumulation in lesions.
  • HHcy increased overall monocyte populations and expanded inflammatory Ly-6C(hi) and Ly-6C(mid) subsets.
  • In vitro, l-homocysteine induced Ly-6C(mid) monocyte differentiation via NAD(P)H oxidase-mediated oxidant stress.

Conclusions:

  • HHcy promotes the differentiation of inflammatory monocyte subsets.
  • HHcy contributes to atherosclerotic lesion development by increasing inflammatory monocyte accumulation.
  • NAD(P)H oxidase-dependent oxidative stress is a key mechanism linking HHcy to monocyte dysfunction in atherosclerosis.
Abstract

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