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High-density lipoprotein inhibits migration of vascular smooth muscle cells through its sphingosine 1-phosphate

Kenichi Tamama1, Hideaki Tomura, Koichi Sato

  • 1Laboratory of Signal Transduction, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512, Japan.

Atherosclerosis
|December 9, 2004
PubMed

Insights

High-density lipoprotein (HDL) prevents atherosclerosis by inhibiting vascular smooth muscle cell migration. Its component, sphingosine 1-phosphate (S1P), plays a key role in this protective mechanism.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cardiovascular Research

Background:

  • High-density lipoprotein (HDL) is recognized for its anti-atherogenic properties.
  • The precise mechanisms underlying HDL's protective effects against atherosclerosis remain incompletely understood.
  • Sphingosine 1-phosphate (S1P) is a bioactive lysolipid mediator found associated with HDL particles.

Purpose of the Study:

  • To investigate the role of HDL-associated S1P in mediating HDL's effects on vascular smooth muscle cells (VSMCs).
  • To elucidate the mechanism by which S1P contributes to the anti-atherogenic actions of HDL.

Main Methods:

  • Experiments involved rat vascular smooth muscle cells (VSMCs) and Chinese hamster ovary (CHO) cells.
  • Assays measured cell migration, cell spreading, and DNA synthesis.
  • S1P receptor (S1P2) expression was manipulated (overexpressed) in CHO cells.
  • VSMC desensitization to S1P was employed to assess response reversibility.

Main Results:

  • Both HDL and S1P significantly inhibited platelet-derived growth factor (PDGF)-induced migration of VSMCs.
  • This inhibitory effect on VSMC migration was linked to reduced cell spreading.
  • S1P-induced desensitization reversed the inhibitory effects of HDL and S1P on VSMC migration.
  • HDL and S1P also inhibited migration in CHO cells, with enhanced effects upon S1P2 receptor overexpression.
  • While S1P promoted DNA synthesis, neither HDL nor S1P increased the overall cell number of VSMCs.

Conclusions:

  • HDL exerts anti-atherogenic effects through its S1P component.
  • S1P mediates the inhibition of VSMC migration and spreading, key processes in atherogenesis.
  • These findings reveal a novel mechanistic pathway for HDL's protective role in cardiovascular health.

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