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Chymase-containing mast cells in human arterial intima: implications for atherosclerotic disease

P T Kovanen1

  • 1Wihuri Research Institute, Helsinki, Finland.

Heart and Vessels
|January 1, 1997
PubMed

Insights

Mast cells containing chymase are found in human atherosclerotic lesions and their activity increases with lesion severity. Chymase may contribute to atherosclerosis development by degrading lipoproteins and destabilizing plaques.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Pathology

Background:

  • Mast cells are present in human atherosclerotic lesions and contain chymase.
  • The number and activity of chymase-containing mast cells increase as atherosclerotic lesions progress.
  • Chymase may play a role in both early and late stages of atherosclerosis.

Purpose of the Study:

  • To investigate the role of chymase in the pathogenesis of atherosclerosis.
  • To explore the mechanisms by which chymase influences lesion development and plaque stability.

Main Methods:

  • Experimental studies using rat serosal mast cells.
  • Analysis of chymase activity on lipoprotein components (apolipoprotein B-100 and apolipoprotein A).
  • Assessment of chymase's effect on macrophage cholesterol content and foam cell formation.
  • Evaluation of chymase's role in activating interstitial procollagenase in plaque caps.

Main Results:

  • Chymase degrades apolipoprotein B-100 in low-density lipoprotein (LDL) particles.
  • Chymase degrades apolipoprotein A in high-density lipoprotein (HDL) particles.
  • These actions increase macrophage cholesterol content, promoting foam cell formation characteristic of early atherosclerotic lesions.
  • Chymase may destabilize atheromatous plaques by activating procollagenase, increasing the risk of cap rupture.

Conclusions:

  • Chymase, released by mast cells in atherosclerotic lesions, contributes to atherogenesis.
  • Chymase promotes the development of early atherosclerotic lesions by modifying lipoproteins and inducing foam cell formation.
  • Chymase may destabilize advanced atherosclerotic plaques, increasing the risk of thrombotic complications.
  • Further research is needed to quantify the role of chymase in atherosclerosis pathogenesis.

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