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1 Walter Reed Army Institute of Research, Silver Spring, Maryland, United States; Medicine, Uniformed Services University of The Health Sciences, Bethesda, Maryland, United States; Pharmacology, Uniformed Services University of The Health Sciences, Bethesda, Maryland, United States
2 US Army Institute of Surgical Research, San Antonio, Texas, United States
3 Pharmacology, Uniformed Services University of The Health Sciences, Bethesda, Maryland, United States
4 Walter Reed Army Institute of Research, Silver Spring, Maryland, United States
5 Walter Reed Army Institute of Research, Silver Spring, Maryland, United States; Medicine, Uniformed Services University of The Health Sciences, Bethesda, Maryland, United States
* To whom correspondence should be addressed. E-mail: juliann.kiang{at}na.amedd.army.mil.
Hemorrhage in mice results in decreased ATP levels in jejunum, lung, kidney, heart, and brain, but not in liver tissue lysates albeit at variable levels and time kinetics. Decreased protein expression and activity of pyruvate dehydrogenase (PDH) accounted for the hemorrhage-induced ATP loss. Treatment with geldanamycin (GA, 1 µg/g body weight), a known inducer of heat shock protein 70 (HSP-70), inhibited the hemorrhage-induced ATP loss in jejunum, lung, heart, kidney, and brain. GA was found to increase PDH protein, preserve PDH enzymatic activity, and inhibit the mucosal injury in jejunum tissues. GA-induced HSP-70i was found to form complexes with PDH protein. HSP-70 gene transfer in to intestinal epithelial cells promoted, whereas HSP-70 siRNA limited the GA-induced increases of PDH and ATP levels. We conclude that agents able to increase expression of HSP-70 and PDH may be of value in reducing pathology resulting from hemorrhage-associated ATP loss.
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