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Effect of macrophage colony stimulating factor on the advanced atherosclerosis in Watanabe heritable hyperlipidemic

Y Watanabe1, T Inaba, H Shimano

  • 13rd Department of Internal Medicine, University of Tokyo, Japan.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|December 24, 1997
PubMed

Insights

Macrophage colony-stimulating factor (M-CSF) did not alter plasma lipids or lesion size in advanced atherosclerosis. However, M-CSF significantly reduced the ratio of intimal to medial thickness in treated rabbits.

Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Biomedical Science

Background:

  • Macrophage colony-stimulating factor (M-CSF) has previously demonstrated a preventative effect on atherosclerosis in young rabbits.
  • The impact of M-CSF on established, advanced atherosclerotic lesions requires further investigation.

Purpose of the Study:

  • To investigate the therapeutic potential of M-CSF in rabbits with established advanced atherosclerosis.
  • To determine if M-CSF influences lipid profiles, aortic cholesterol ester content, lesion area, or vascular wall remodeling in advanced atherosclerosis.

Main Methods:

  • Recombinant human M-CSF was administered to 11-month-old WHHL rabbits with established atherosclerosis three times weekly for 8 months.
  • Plasma lipid levels, aortic cholesterol ester content, and macroscopic lesion area were assessed.
  • The ratio of intimal to medial thickness was measured to evaluate vascular remodeling.

Main Results:

  • No significant differences were observed in plasma lipid levels, aortic cholesterol ester content, or macroscopic atherosclerosis lesion area between M-CSF treated and control groups.
  • A significant reduction in the intimal to medial thickness ratio was observed in the M-CSF treated group compared to controls (1.08 vs 1.7, p < 0.01).

Conclusions:

  • M-CSF treatment did not affect established atherosclerotic plaque size or lipid profiles in WHHL rabbits.
  • M-CSF may modulate vascular smooth muscle cell function, influencing vascular remodeling even in advanced atherosclerotic lesions.

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