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LXR-Mediated ABCA1 Expression and Function Are Modulated by High Glucose and PRMT2

Maryem A Hussein1, Elina Shrestha1, Mireille Ouimet2

  • 1Department of Microbiology, NYU School of Medicine, New York, New York, United States of America.

Plos One
|August 20, 2015
PubMed

Insights

High glucose impairs atherosclerosis regression by reducing Protein Arginine Methyltransferase 2 (PRMT2). This impacts Liver X Receptor (LXR)-dependent cholesterol transporter ABCA1 expression, offering insights into diabetes-related atherosclerosis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Science

Background:

  • Atherosclerosis, a major risk factor for cardiovascular disease, is exacerbated by high cholesterol and diabetes.
  • Liver X Receptor (LXR) activation promotes cholesterol efflux, crucial for atherosclerosis regression.
  • Diabetes impairs atherosclerosis regression, suggesting glucose dysregulation affects LXR-mediated processes.

Purpose of the Study:

  • To investigate how glucose levels modulate Liver X Receptor (LXR)-dependent gene expression in macrophages.
  • To identify molecular mechanisms underlying impaired atherosclerosis regression in diabetes.

Main Methods:

  • Utilized mouse macrophage cell lines (RAW 264.7) and primary bone marrow-derived macrophages (BMDMs).
  • Cultured cells in normal and high glucose conditions mimicking diabetes.
  • Assessed LXR-dependent gene expression, including ATP-binding cassette transporter A1 (ABCA1) and ABCG1.
  • Examined the expression of chromatin-modifying enzymes, focusing on Protein Arginine Methyltransferase 2 (PRMT2).
  • Compared ABCA1 expression and cholesterol efflux in wild-type and Prmt2 knockout (Prmt2-/-) macrophages.
  • Analyzed monocyte PRMT2 expression in diabetic and non-diabetic mice.

Main Results:

  • High glucose significantly inhibited LXR-dependent ATP-binding cassette transporter A1 (ABCA1) expression, but not ABCG1.
  • Protein Arginine Methyltransferase 2 (PRMT2) expression was reduced under high glucose conditions.
  • Macrophages lacking PRMT2 (Prmt2-/-) exhibited reduced ABCA1 expression and impaired ABCA1-mediated cholesterol efflux.
  • Diabetic mouse monocytes displayed decreased PRMT2 expression compared to non-diabetic controls.

Conclusions:

  • Protein Arginine Methyltransferase 2 (PRMT2) is a glucose-sensitive factor involved in regulating ABCA1 expression and cholesterol efflux.
  • Reduced PRMT2 under high glucose conditions contributes to impaired LXR-mediated cholesterol transport.
  • These findings provide a molecular link between diabetes, PRMT2 deficiency, and increased atherosclerosis risk.

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