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Lipoproteins modulate expression of the macrophage scavenger receptor

J Han1, A C Nicholson

  • 1Department of Pathology, Cornell University Medical College, New York, New York 10021, USA.

Insights

Lipoproteins, including oxidized LDL (OxLDL), significantly increase macrophage scavenger receptor (MSR) mRNA expression. This suggests lipoproteins may worsen foam cell development in atherosclerosis.

Area of Science:

  • Biochemistry
  • Immunology
  • Cell Biology

Background:

  • Macrophage scavenger receptors (MSR) internalize oxidized low-density lipoprotein (OxLDL), a key lipid source in atherosclerotic lesions.
  • The influence of lipoproteins on MSR expression remains unclear.

Purpose of the Study:

  • To investigate the effect of native and modified LDL on MSR expression in macrophages.
  • To determine the regulatory mechanisms of MSR expression by lipoproteins.

Main Methods:

  • RAW cells and primary murine macrophages were treated with various LDL preparations (native, acetylated, oxidized).
  • MSR mRNA expression was quantified using RT-PCR.
  • Macrophage scavenger receptor function was assessed via 125I-AcLDL binding assays.
  • MSR mRNA stability was evaluated.
  • Peritoneal macrophages were isolated from lipoprotein-injected mice.

Main Results:

  • Lipoprotein exposure, particularly OxLDL and acetylated LDL (AcLDL), markedly induced MSR mRNA expression (12- to 17-fold) in RAW cells.
  • OxLDL and native LDL peaked MSR mRNA induction at 1 hour, while AcLDL showed a delayed secondary peak.
  • Scavenger receptor function showed only modest increases.
  • Cholesterol acceptor treatment decreased MSR mRNA expression, correlating with cholesterol loss.
  • OxLDL did not affect MSR mRNA stability, indicating transcriptional regulation.
  • In vivo, LDL, AcLDL, and OxLDL significantly increased MSR mRNA in peritoneal macrophages (16-fold).

Conclusions:

  • Lipoproteins, including OxLDL and AcLDL, transcriptionally upregulate macrophage scavenger receptor (MSR) expression.
  • Increased MSR expression by lipoproteins may contribute to lipid accumulation and foam cell formation in atherosclerosis.

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