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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
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.
Aim:
To investigate the presence of membrane "flip flop" in ischaemic human myocardium, we assessed depositions of apolipoprotein H (apoH; beta 2-glycoprotein 1) in ischaemic myocardium. Serum protein apoH can bind to negatively charged phospholipids and can also inhibit blood coagulation in vitro. We hypothesised that, because of its affinity for phosphatidyl serine, apoH might bind to "flip flopped" cells and would therefore be useful as a marker for membrane flip flop in vivo.
Methods:
Myocardial tissue specimens were obtained from patients who had died within 14 days of acute myocardial infarction.
Results:
Immunohistochemical analysis of these specimens revealed that apoH was selectively deposited in infarcted areas of human myocardium of at least one day's duration. Depositions of apoH were not found in non-ischaemic myocardial tissue samples obtained from patients who died from other (extracardial) causes. In vitro experiments with the human leukaemia T cell line Jurkat, subjected to apoptosis by etoposide, showed that apoH was bound to the membrane of apoptotic cells. However, these experiments also indicated that flip flop itself is not sufficient for apoH binding. In addition, Jurkat cells that bound apoH were positive for activated complement complexes, as was also found in the human heart.
Conclusions:
These results suggest that apoH is involved in the inflammatory processes that occur in ischaemic myocardium.