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1 Pathology, VU Medical Center, Amsterdam, The Netherlands; ICaR-VU, Amsterdam, The Netherlands
2 Pathology, VU Medical Center, Amsterdam, The Netherlands
3 Immunopathology, Sanquin Research at CLB, Amsterdam, The Netherlands
4 Physiology, VU Medical Center, Amsterdam, The Netherlands; ICaR-VU, Amsterdam, The Netherlands
5 Cardiology, VU Medical Center, Amsterdam, The Netherlands; ICaR-VU, Amsterdam, The Netherlands
6 Clinical Chemistry, VU Medical Center, Amsterdam, The Netherlands; ICaR-VU, Amsterdam, The Netherlands; Immunopathology, Sanquin Research at CLB, Amsterdam, The Netherlands
* To whom correspondence should be addressed. E-mail: paj.krijnen{at}vumc.nl.
We examined the relationship between clusterin and activated complement in human heart infarction and evaluated the effect of this protein on ischemic rat neonatal cardiomyoblasts (H9c2)and isolated adult ventricular rat cardiomyocytes, as an in vitro models of acute myocardial infarction. Clusterin protects cells by inhibiting complement and co-localizes with complement on jeopardized human cardiomyocytes after infarction. The distribution of clusterin and complement factor C3d was evaluated in the infarcted human heart. We also analyzed protein expression of clusterin in ischemic H9c2 cells. The binding of endogenous- and purified human clusterin on H9c2 cells was analyzed by Flow Cytometry. Furthermore, the effect of clusterin on the viability of ischemically challenged H9c2 cells and isolated adult ventricular rat cardiomyocytes was analyzed. In human myocardial infarcts, clusterin was found on scattered, morphologically viable cardiomyocytes within the infarcted area, that were negative for complement. In H9c2 cells, clusterin was rapidly expressed upon ischemia. Its expression was reduced after reperfusion. Clusterin bound to single-annexin V-positive or annexin V/propidium iodide-positive H9c2 cells. Clusterin inhibited ischemia induced death in H9c2 cells as well as in isolated adult ventricular rat cardiomyocytes in the absence of complement. We conclude that ischemia induces up-regulation of clusterin in ischemically challenged, but viable cardiomyocytes. Our data suggests that clusterin protects cardiomyocytes against ischemic cell death via a complement independent pathway.
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