This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Swertfeger, D. K. Articles by Harmony, J. A. Search for Related Content PubMed PubMed Citation Articles by Swertfeger, D. K. Articles by Harmony, J. A.

American Journal of Pathology, Vol 148, 1971-1983, Copyright © 1996 by American Society for Investigative Pathology

REGULAR ARTICLES

Apolipoprotein J/clusterin induction in myocarditis: A localized response gene to myocardial injury

DK Swertfeger, DP Witte, WD Stuart, HA Rockman and JA Harmony
Developmental Biology Graduate Program, University of Cincinnati, College of Medicine, Cincinnati, 45267, USA.

The function of apolipoprotein J (apoJ) is unknown, but it has been hypothesized to be cytoprotective. In the normal heart, abundant apoJ mRNA and protein are expressed in atrial myocytes; no expression is detected in ventricular myocytes. To provide clues about the role of apoJ in the heart, the response of apoJ to heart disease, including three models of myocarditis and two models of in vivo pressure overload hypertrophy, were examined. In the disease model studied extensively, myosin-induced myocarditis, in situ hybridization detected induction of apoJ mRNA in ventricular myocytes immediately before histological evidence of injury. ApoJ message in ventricular myocytes reached high levels as myocarditis became more severe. Evidence of early apoJ induction, before inflammation and injury, also occurred in viral myocarditis. ApoJ mRNA was not present in the inflammatory or interstitial cells during myocarditis. In areas of severe inflammation and myocardial fiber degeneration, apoJ showed a gradient of expression, with highest levels in myocytes immediately surrounding the lesion and diminishing with increasing distance. ApoJ protein also accumulated in myocytes at the interface between degenerated myocardial tissue and the surrounding cardiac tissue. During cardiac hypertrophy that occurred without associated inflammation or cell damage, ventricular apoJ mRNA was not detected. When ischemic damage accompanied hypertrophy, apoJ was induced in the ventricular myocytes near the lesion borders. The correlation of apoJ induction with ventricular tissue damage, but not hypertrophy, suggests that apoJ is a repair response protein. We propose that apoJ functions to limit tissue injury and/or promote tissue remodeling.

This article has been cited by other articles:

				P. A. J. Krijnen, S. A. G. M. Cillessen, R. Manoe, A. Muller, C. A. Visser, C. J. L. M. Meijer, R. J. P. Musters, C. E. Hack, L. A. Aarden, and H. W. M. Niessen Clusterin: a protective mediator for ischemic cardiomyocytes? Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H2193 - H2202. [Abstract] [Full Text] [PDF]

				M. Miyata, S. Biro, H. Kaieda, H. Eto, K. Orihara, T. Kihara, H. Obata, N. Matsushita, T. Matsuyama, and C. Tei Apolipoprotein J/Clusterin Is Induced in Vascular Smooth Muscle Cells After Vascular Injury Circulation, September 18, 2001; 104(12): 1407 - 1412. [Abstract] [Full Text] [PDF]

				D.-J. Choi, W. J. Koch, J. J. Hunter, and H. A. Rockman Mechanism of beta -Adrenergic Receptor Desensitization in Cardiac Hypertrophy Is Increased beta -Adrenergic Receptor Kinase J. Biol. Chem., July 4, 1997; 272(27): 17223 - 17229. [Abstract] [Full Text] [PDF]