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Am J Physiol Heart Circ Physiol 282: H1672-H1678, 2002; doi:10.1152/ajpheart.00955.2001
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Vol. 282, Issue 5, H1672-H1678, May 2002

Targeted myocardial transgenic expression of HIV Tat causes cardiomyopathy and mitochondrial damage

Scott M. Raidel1, Chad Haase1, Natalie R. Jansen1, Rodney B. Russ1, Roy L. Sutliff1, Leonard W. Velsor2, Brian J. Day2, Brian D. Hoit3, Allen M. Samarel4, and William Lewis1

1 Emory University School of Medicine, Atlanta, Georgia 30322; 2 National Jewish Medical Center, Denver, Colorado 80206; 3 University Hospital Cleveland, Cleveland, Ohio 44106; 4 Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois 60153

Cardiac effects of human immunodeficiency virus (HIV) transactivator (Tat) are unclear, but Tat decreases liver glutathione (an important mitochondrial antioxidant) when ubiquitously expressed in transgenic mice (TG). With an alpha -myosin heavy chain promoter, Tat was selectively targeted to murine cardiac myocytes. One high-expression hemizygous (+/-Tathigh; 12 copies) and two low-expression (+/-TatlowA,B; 2-5 copies) TG lines were created. Cardiomyopathy was documented with increased left ventricle (LV) mass, ventricular expression of atrial natriuretic factor (ANF) mRNA, mitochondrial ultrastructural defects, and myocardial depletion of glutathione. In +/-Tathigh TGs, normalized LV mass (determined echocardiographically) increased 46% (90 days), 134% (240 days), and 96% (365 days) compared with wild-type littermates (WT). LV fractional shortening was decreased to 28% (90 days), 27% (240 days), and 19% (365 days). +/-Tatlow LV mass was unchanged (<= 365 days). ANF in +/-Tathigh ventricles (180 days) was twofold WT values. Glutathione was selectively decreased in +/-Tathigh hearts (120 days). +/-Tathigh hearts contained damaged mitochondria (>= 210 days); however, profound mitochondrial destruction occurred in homozygous +/+Tathigh hearts (10 days) and the pups died (14 days). Tat caused cardiac dysfunction in this TG and may impact on cardiomyopathy in acquired immunodeficiency syndrome.

acquired immunodeficiency syndrome; cardiac dysfunction; echocardiogram; oxidative stress; transmission electron microscopy


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