Temporal induction of clusterin in the peri-infarct zone after experimental myocardial infarction in the rat

John R. Silkensen, Alan T. Hirsch, Mary M. Lunzer, David Chmielewski, J. Carlos Manivel, Michael R. Muellerleile, Mark E. Rosenberg

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17 Scopus citations


Cluster, a glycoprotein with potent cellular cohesive properties, is induced in many organs at times of tissue injury or remodeling. After renal infarction, for example, clusterin is localized to tubular epithelial cells in the peri-infarct zone. The purpose of this study was to examine the spatial and temporal expression of cardiac clusterin after myocardial infarction. Sprague-Dawley rats underwent permanent coronary ligation or sham operation. Hearts were harvested at 6 hours and at 2, 14, and 28 days after infarction. Cardiac clusterin expression was examined by immunohistochemistry and in situ hybridization. Left ventricular clusterin staining was evident at 6 hours and 2 days after myocardial infarction, although not at later time periods. Clusterin was localized to peri-infarct zone myocytes and endothelial cells of this region, and local synthesis of clusterin by myocytes was confirmed by in situ hybridization. Clusterin was not present in inflammatory cells or in left ventricular tissue distant from the infarct. The distribution of clusterin was different from the membrane attack complex of complement (C5b-9), with the latter being present diffusely throughout the infarct zone. Although the role of cardiac clusterin is not known, we speculate that clusterin's cohesive properties serve to promote myocyte interactions that are perturbed in the peri-infarct zone after myocardial infarction.

Original languageEnglish (US)
Pages (from-to)28-35
Number of pages8
JournalJournal of Laboratory and Clinical Medicine
Issue number1
StatePublished - Jan 1998

Bibliographical note

Funding Information:
From the Departments of Medicine and Laboratory Medicine and Pathology, University of Minnesota. Supported by Public Health Service Grant R29DK43075 (M.E.R.); by Cfinical Investigator Award 5K08-HL02429 from the National Heart, Lung, and Blood Institute (A.T.H.); by a National Resarch Service Award (J.R.S.); and by the Baxter Extramural Grant Program. This work was done during the tenure of an Established Investigatorship from the American Heart Association (M.E.R.). Submitted for publication June 10, 1996; revision submitted Aug. 7, 1997; accepted Aug. 15, 1997. Reprint requests: John R. Silkensen, MD, University of Minnesota Department of Medicine, Box 736 UMHC, 516 Delaware Street SE, Minneapolis, MN 55455.


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