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Am J Physiol Heart Circ Physiol 281: H1035-H1039, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 3, H1035-H1039, September 2001

TGF-beta 1 modulates NOS expression and phosphorylation of Akt/PKB in rat myocytes exposed to hypoxia-reoxygenation

Hongjiang Chen1, Dayuan Li1, Tom Saldeen2, and Jawahar L. Mehta1

1 Department of Medicine and Physiology, University of Arkansas and Central Arkansas Veterans Health Care System, Little Rock, Arkansas 72205-7199; and 2 Department of Forensic Medicine, University of Uppsala, Uppsala, Sweden S-752-37

Myocardial hypoxia-reoxygenation (H-R) is associated with upregulation of inducible nitric oxide synthase (iNOS), decrease in endothelial NOS (eNOS), and increase in protein kinase B (PKB). Previous work also shows that transforming growth factor-beta 1 (TGF-beta 1) can attenuate myocardial injury induced by H-R. We examined the modulation of NOS and PKB expression in response to H-R by TGF- beta 1. Myocytes from Sprague-Dawley rat hearts were cultured and exposed to hypoxia (95% N2-5% CO2, PO2 ~30 mmHg) for 24 h and reoxygenation (95% air-5% CO2) for 3 h. Myocytes were then examined for lactate dehydrogenase (LDH) release, iNOS activity (conversion of L-[3H]arginine to L-[3H]citrulline), iNOS and eNOS expression, and PKB phosphorylation. H-R alone resulted in myocyte injury, upregulation of iNOS activity and expression, decrease in eNOS expression, and increase in PKB phosphorylation (all P < 0.05 vs. cells cultured in normoxic conditions). Treatment of myocytes with TGF-beta 1 (1 ng/ml) resulted in a reduction in LDH release, attenuation of the alterations in NOS expression (both iNOS and eNOS), and PKB phosphorylation in response to H-R (all P < 0.05 vs. H-R alone). These observations suggest that TGF-beta 1 decreases H-R injury and attenuates alterations in NOS and PKB phosphorylation in myocytes exposed to H-R.

nitric oxide; protein kinase B; transforming growth factor; apoptosis; endothelium


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