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Homocysteine accelerates atherosclerosis by inhibiting scavenger receptor class B member1 via DNMT3b/SP1 pathway

Wei Guo1, Huiping Zhang2, Anning Yang1

  • 1Department of Pathology and Pathophysiology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China; Ningxia Key Laboratory of Vascular Injury and Repair Research, Yinchuan, China; NHC Key Laboratory of Metabolic Cardiovascular Diseases Research (NingXia Medical University), Yinchuan, China.

Journal of Molecular and Cellular Cardiology
|November 17, 2019
PubMed

Insights

High homocysteine (Hcy) accelerates atherosclerosis by reducing scavenger receptor class B member 1 (SCARB1). DNA methyltransferase 3 beta (DNMT3b) inhibits SCARB1, promoting lipid accumulation in foam cells.

Area of Science:

  • Cardiovascular Biology
  • Epigenetics
  • Atherosclerosis Research

Background:

  • Homocysteine (Hcy) is a risk factor for atherosclerosis, characterized by lipid accumulation.
  • Scavenger receptor class B member 1 (SCARB1) is protective against atherosclerosis, but its role in Hcy-mediated disease is unclear.

Purpose of the Study:

  • To elucidate the mechanism of SCARB1 in Hcy-induced atherosclerosis.
  • To investigate the epigenetic regulation of SCARB1 by Hcy.

Main Methods:

  • Assessed SCARB1 expression in atherosclerotic plaques and Hcy-treated foam cells.
  • Investigated the effect of SCARB1 overexpression on lipid accumulation.
  • Analyzed SCARB1 promoter methylation and SP1 binding.
  • Examined the role of DNMT3b in regulating SCARB1.

Main Results:

  • SCARB1 expression was significantly inhibited in atherosclerotic plaques and Hcy-treated foam cells.
  • SCARB1 overexpression suppressed lipid accumulation in Hcy-treated foam cells.
  • Hcy treatment did not alter SCARB1 promoter methylation.
  • DNMT3b inhibited SCARB1 expression by reducing SP1 recruitment to the SCARB1 promoter.

Conclusions:

  • DNMT3b-induced inhibition of SCARB1 accelerates Hcy-mediated atherosclerosis.
  • This acceleration is linked to increased lipid accumulation in foam cells due to reduced SP1 binding to the SCARB1 promoter.
  • Findings offer insights into an epigenetic mechanism underlying atherosclerosis.

Keywords:
AtherosclerosisDNMT3bHomocysteineSCARB1SP1

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