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Hyperhomocysteinemia potentiates hyperglycemia-induced inflammatory monocyte differentiation and atherosclerosis

Pu Fang1, Daqing Zhang1, Zhongjian Cheng1

  • 1Center for Metabolic Disease Research, School of Medicine, Temple University, Philadelphia, PA Department of Pharmacology, School of Medicine, Temple University, Philadelphia, PA.

Diabetes
|July 11, 2014
PubMed

Insights

High homocysteine (HHcy) and hyperglycemia (HG) accelerate atherosclerosis by promoting inflammatory cell differentiation. Lowering homocysteine levels reversed these effects, suggesting a role for DNA hypomethylation.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Diseases
  • Atherosclerosis Research

Background:

  • Hyperhomocysteinemia (HHcy) is linked to diabetic cardiovascular complications.
  • The specific role of HHcy in hyperglycemia-driven (HG) atherogenesis is not well understood.
  • Understanding this interaction is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the mechanisms by which HHcy exacerbates HG-induced atherosclerosis.
  • To determine the impact of HHcy and HG on inflammatory cell populations.
  • To explore the potential of homocysteine-lowering as a therapeutic strategy.

Main Methods:

  • Established a mouse model with both HHcy and HG susceptibility.
  • Utilized cystathionine β-synthase deficient mice with inducible human CBS (Tg-hCBS) for homocysteine control.
  • Induced hyperglycemia via streptozotocin and atherosclerosis via high-fat diet in ApoE(-/-) mice.

Main Results:

  • Combined HHcy and HG significantly accelerated atherosclerosis, increasing lesion monocytes (MCs) and macrophages (MØs).
  • Homocysteine-lowering treatments reversed elevated circulating mononuclear cells and inflammatory MC/MØ levels.
  • l-homocysteine and d-glucose promoted inflammatory MC differentiation, linked to DNA hypomethylation.

Conclusions:

  • HHcy and HG synergistically accelerate atherosclerosis and inflammatory cell differentiation.
  • DNA hypomethylation is a key mechanism underlying these effects.
  • Reversing HHcy shows therapeutic potential in mitigating HG-associated cardiovascular risk.

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