APOLIPOPROTEIN J CLUSTERIN INDUCTION IN MYOCARDITIS/

The function of apolipoprotein J (apoJ) is unknown, but it has been hy pothesized to be cytoprotective. In the normal heart, abundant apoJ mR NA and protein are expressed in atrial myocytes; no expression is dete cted in ventricular myocytes. To provide clues about the role of apoJ in the heart, the response of apoJ to heart disease, including three m odels of myocarditis and two models of in vivo pressure overload hyper trophy, 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 a s myocarditis became more severe. Evidence of early apoJ induction, be fore 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 deg eneration, apoJ showed a gradient of expression, with highest levels i n myocytes immediately surrounding the lesion and diminishing with inc reasing distance. ApoJ protein also accumulated in myocytes at the int erface between degenerated myocardial tissue and the surrounding cardi ac tissue During cardiac hypertrophy that occurred without associated inflammation or cell damage, ventricular apoJ mRNA was not detected Wh en ischemic damage accompanied hypertrophy, apoJ was induced in the ve ntricular myocytes near the lesion borders. The correlation of apoJ in duction 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.