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P38 MAP kinase regulates negative inotropic effect of HIV gp120 on cardiac myocytes through Troponin I phosphorylation


, : P38 MAP kinase regulates negative inotropic effect of HIV gp120 on cardiac myocytes through Troponin I phosphorylation. FASEB Journal 16(4): A570, March 20

Myocardial dysfunction leading to dilated cardiomyopathy (DCM) has been documented with surprisingly high frequency in HIV infected individuals. Potential pathophysiologic mechanisms include indirect effects mediated by cytokines and/or direct effects of HIV on cardiac myocyte function. We recently reported that the HIV coat protein, gp120, enhanced IL-1b induced NO production in neonatal rat cardiac myocytes through a novel p38 MAP kinase mechanism (Am J Phys 279:H3138-3143, 2000). We now report the direct effects of HIV gp120 alone on isolated adult rat ventricular myocytes (ARVM). ARVM were continuously superfused with gp120 (1mg/ml) and percentage fractional shortening (FS) determined by automated border detection and simultaneous (Ca++)i measured by fura-2AM (2mM) fluorescence. Gp120 alone increased FS and increased (Ca++)i at 2-20 min and then depressed FS with no change in (Ca++)i at 1-2 hrs (N=9; p<0.01). P38 MAP kinase activation was noted at 10 min to 2 hrs associated with phosphorylation of Troponin I (Tn I). Inhibition of p38 MAP kinase activation and Tn I phosphorylation by SB203580 completely prevented the delayed negative inotropic effect of gp120 (N=9; p<0.01). We conclude that HIV gp120 directly regulates ARVM through an initial Ca++ dependent positive inotropic effect followed by a Ca++ independent negative inotropic effect mediated by p38 MAP kinase phosphorylation of Tn I.

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