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A20 alleviates the vascular remodeling induced by homocysteine

Liang Chen1,2, Lei Lei1,2, Tianyu Li3

  • 1Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan 430030, Hubei Province, China.

American Journal of Translational Research
|January 22, 2019
PubMed

Insights

High homocysteine levels contribute to cardiovascular disease by promoting vascular remodeling. A20 protein plays a protective role by suppressing inflammation and smooth muscle cell proliferation.

Area of Science:

  • Cardiovascular Science
  • Molecular Biology
  • Pathophysiology

Background:

  • Hyperhomocysteinemia is a known risk factor for cardiovascular diseases.
  • The precise mechanisms of homocysteine-induced vascular remodeling remain unclear.

Purpose of the Study:

  • To elucidate the role of A20 in homocysteine-induced vascular remodeling.
  • To investigate the molecular pathways involved in this process.

Main Methods:

  • Established a hyperhomocysteinemia mouse model using a high L-methionine diet.
  • Utilized in vivo and in vitro experiments to assess macrophage accumulation, VSMC proliferation/migration, and A20 expression.
  • Investigated the effects of A20 overexpression and downregulation on cellular responses to homocysteine.
  • Analyzed the involvement of NF-kappaB, IRF3, and PPAR-γ signaling pathways.

Main Results:

  • High methionine diet induced macrophage accumulation, VSMC proliferation, and decreased A20 expression in mouse aortas.
  • A20 overexpression suppressed NF-kappaB p65 nuclear translocation and attenuated homocysteine-induced VSMC proliferation and migration.
  • A20 downregulation reversed these protective effects.
  • A20 alleviated vascular remodeling by reducing inflammation and VSMC proliferation/migration via IRF3 and PPAR-γ.

Conclusions:

  • A20 plays a critical protective role against homocysteine-induced vascular remodeling.
  • A20 exerts its effects by modulating inflammatory responses and VSMC behavior through specific molecular pathways.

Keywords:
A20IRF3PPAR-γhomocysteineproliferation and migration

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