Biochem Biophys Res Commun. 2004 May 7;317(3):801-10.

Regulation of the SM-20 prolyl hydroxylase gene in smooth muscle cells.

Menzies K, Liu B, Kim WJ, Moschella MC, Taubman MB.

Source

The Zena and Michael A. Wiener Cardiovascular Institute, Department of Medicine, The Mount Sinai School of Medicine, New York, NY 10029, USA.

Abstract

SM-20 encodes an intracellular prolyl hydroxylase that acts on hypoxia inducible factor (HIF)-1alpha, targeting it for proteasomal degradation. By decreasing HIF-alpha, SM-20 is thought to modulate the expression of hypoxia-regulated genes. SM-20 expression in the arterial wall is restricted to smooth muscle cells, which play a critical role in atherosclerosis and arterial injury. To further elucidate the regulation of SM-20 in smooth muscle, we cloned and analyzed the rat SM-20 promoter. In transient transfections, the SM-20 promoter displayed approximately 6-fold greater activity in smooth muscle cells vs. fibroblasts. Deletion analysis and electrophoretic mobility shift assays demonstrated that SM-20 transcription was regulated by two Sp1/Sp3 sites. A shift in binding to the Sp1/Sp3 sites, a decrease in Sp1 and Sp3 protein levels, and the emergence of a lower molecular weight form of Sp1 were seen in serum-deprived or post-confluent SMC, suggesting that SM-20 is regulated during smooth muscle cell differentiation.

PMID:: 15081411; [PubMed - indexed for MEDLINE]

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