Co-deposition of clusterin with the complement membrane attack complex in myocardial infarction.

Clusterin is a multi-functional plasma glycoprotein that has been shown to inhibit formation of the complement membrane attack complex (MAC) by preventing the association of terminal complement complexes with target cell membranes. Recent studies have suggested that complement activation is involved in the development of tissue injury of myocardial infarction. In this study we observed that clusterin is selectively deposited in the infarcted areas of human myocardium. Clusterin deposits were observed in the heart tissue of 10 patients whose infarcted lesions were 8 hr to 14 days old, but not in patients who died from other causes. Clusterin co-localized with the MAC on the surface of damaged cardiomyocytes. In normal myocardium only endothelial lining of blood vessels occasionally stained positive for clusterin. The 80,000 MW clusterin was also detected by Western blot analysis in extracts of myocardial infarction lesions, but only faintly in extracts of normal heart. As clusterin has apparently failed in protecting myocardium against complement-mediated cell injury its main role might be to participate in the clearance of damaged and necrotic tissue together with the MAC.