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Lipoprotein(a) in atherosclerotic plaques recruits inflammatory cells through interaction with Mac-1 integrin

Sotirios N Sotiriou1, Valeria V Orlova, Nadia Al-Fakhri

  • 1Experimental Immunology Branch, NCI, NIH, Bethesda, Maryland 20892, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|January 13, 2006
PubMed

Insights

Lipoprotein(a) [Lp(a)] promotes atherosclerosis by enhancing inflammatory cell recruitment. Its apolipoprotein(a) binds Mac-1, increasing monocyte adhesion and migration, a key step in plaque development.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Atherosclerosis Research

Background:

  • Lipoprotein(a) [Lp(a)] is a known risk factor for atherosclerotic disorders.
  • The precise mechanisms underlying Lp(a)-mediated atherogenicity remain incompletely understood.

Purpose of the Study:

  • To elucidate a novel function of Lp(a) in promoting inflammatory cell recruitment.
  • To define the molecular interactions and pathways through which Lp(a) contributes to atherogenesis.

Main Methods:

  • Investigated Lp(a) interaction with the beta2-integrin Mac-1.
  • Assessed monocyte adhesion and transendothelial migration.
  • Analyzed NF-kappaB activation and tissue factor expression.
  • Examined Lp(a) and Mac-1 localization in atherosclerotic coronary arteries.

Main Results:

  • Lp(a) specifically binds to Mac-1 via its apolipoprotein(a) [apo(a)] moiety, promoting monocyte adhesion and migration.
  • This interaction is enhanced by homocysteine and inhibited by plasminogen/angiostatin kringle 4.
  • Lp(a)-Mac-1 interaction triggers NF-kappaB activation and prothrombotic tissue factor expression.
  • Co-localization of Lp(a) and Mac-1 was observed on mononuclear cells within atherosclerotic arteries.

Conclusions:

  • Lp(a) acts as a ligand for Mac-1, facilitating inflammatory cell recruitment to atherosclerotic plaques.
  • This novel mechanism highlights Lp(a)'s role in atherogenicity through immune cell infiltration.
  • Findings provide new insights into the molecular basis of Lp(a)-associated cardiovascular risk.

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