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Am J Physiol Cell Physiol 280: C1176-C1183, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 5, C1176-C1183, May 2001

Acidification and glucocorticoids independently regulate branched-chain alpha -ketoacid dehydrogenase subunit genes

X. Wang1, J. M. Chinsky2,3, P. A. Costeas2, and S. Russ Price1

1 Renal Division, Emory University School of Medicine, Atlanta, Georgia 30322; 2 Division of Human Genetics, Department of Pediatrics, University of Maryland School of Medicine, Baltimore 21201, and 3 Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287

Acidification or glucocorticoids increase the maximal activity and subunit mRNA levels of branched chain alpha -ketoacid dehydrogenase (BCKAD) in various cell types. We examined whether these stimuli increase transcription of BCKAD subunit genes by transfecting BCKAD subunit promoter-luciferase plasmids containing the mouse E2 or human E1alpha -subunit promoter into LLC-PK1 cells, which do not express glucocorticoid receptors, or LLC-PK1-GR101 cells, which we have engineered to constitutively express the glucocorticoid receptor gene. Dexamethasone or acidification increased luciferase activity in LLC-PK1-GR101 cells transfected with the E2 or E1alpha -minigenes; acidification augmented luciferase activity in LLC-PK1 cells transfected with these minigenes but dexamethasone did not. A pH-responsive element in the E2 subunit promoter was mapped to a region >4.0 kb upstream of the transcription start site. Dexamethasone concurrently stimulated E2 subunit promoter activity and reduced the binding of nuclear factor-kappa B (NF-kappa B) to a site in the E2 promoter. Thus acidification and glucocorticoids independently enhance BCKAD subunit gene expression, and the glucocorticoid response in the E2 subunit involves interference with NF-kappa B, which may act as a transrepressor.

acidosis; branched-chain amino acids; gene expression; branched-chain ketoacid dehydrogenase


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