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Apolipoprotein H, a new mediator in the inflammatory changes ensuring in jeopardised human myocardium

H W Niessen1, W K Lagrand, H J Rensink

  • 1Department of Pathology, Free University Hospital, PO Box 7057, De Boelelaaan 1117, 1081 HV Amsterdam, The Netherlands. jwm.niessen@azvu.nl

Journal of Clinical Pathology
|December 29, 2000
PubMed

Insights

Apolipoprotein H (apoH) deposits in ischaemic heart tissue suggest its role in inflammation. ApoH binding to cells indicates it may serve as a marker for cellular damage in myocardial infarction.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Cell Biology

Background:

  • Membrane asymmetry is crucial for cell function.
  • Disruption of membrane asymmetry, or "flip flop", occurs in cellular injury.
  • Apolipoprotein H (apoH) binds negatively charged phospholipids, including phosphatidyl serine.

Purpose of the Study:

  • To investigate membrane "flip flop" in human ischaemic myocardium.
  • To assess the deposition of apolipoprotein H (apoH) as a potential marker for membrane flip flop in vivo.
  • To explore the role of apoH in the inflammatory response to myocardial infarction.

Main Methods:

  • Immunohistochemical analysis of myocardial tissue from patients post-myocardial infarction.
  • In vitro experiments using the Jurkat T cell line subjected to apoptosis.
  • Assessment of apoH binding to apoptotic cells and activated complement complexes.

Main Results:

  • ApoH was selectively deposited in infarcted areas of human myocardium.
  • ApoH deposition was absent in non-ischaemic myocardial tissue.
  • In vitro, apoH bound to apoptotic cells, but flip flop alone was insufficient for binding; activated complement complexes were also present.

Conclusions:

  • Apolipoprotein H (apoH) is involved in the inflammatory processes within ischaemic myocardium.
  • ApoH may serve as a biomarker for cellular damage and inflammation following myocardial infarction.
  • Further research is warranted to elucidate the precise mechanisms of apoH involvement in myocardial inflammation.
Abstract

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