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Research Article Free access | 10.1172/JCI114504

Dihydropyridine receptor gene expression is regulated by inhibitors of myogenesis and is relatively insensitive to denervation.

H T Shih, M S Wathen, H B Marshall, J M Caffrey, and M D Schneider

Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.

Find articles by Shih, H. in: JCI | PubMed | Google Scholar

Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.

Find articles by Wathen, M. in: JCI | PubMed | Google Scholar

Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.

Find articles by Marshall, H. in: JCI | PubMed | Google Scholar

Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.

Find articles by Caffrey, J. in: JCI | PubMed | Google Scholar

Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.

Find articles by Schneider, M. in: JCI | PubMed | Google Scholar

Published March 1, 1990 - More info

Published in Volume 85, Issue 3 on March 1, 1990
J Clin Invest. 1990;85(3):781–789. https://doi.org/10.1172/JCI114504.
© 1990 The American Society for Clinical Investigation
Published March 1, 1990 - Version history
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Abstract

To evaluate developmental and physiological signals that may influence expression of the dihydropyridine-sensitive "slow" Ca2+ channel, we analyzed dihydropyridine receptor (DHPR) mRNA abundance in mouse skeletal muscle. Using synthetic oligonucleotide probes corresponding to the rabbit skeletal muscle DHPR, a 6.5 kb DHPR transcript was identified in postnatal skeletal muscle and differentiated C2 or BC3H1 myocytes, but not cardiac muscle or brain. DHPR gene expression was reversibly suppressed by 0.4 nM transforming growth factor beta-1 or by transfection with a mutant c-H-ras allele, nominal inhibitors of myogenesis that block the appearance of slow channels and DHPR. In contrast, both BC3H1 and C2 myocytes containing the activated ras vector expressed the gene encoding the nicotinic acetylcholine receptor delta subunit, demonstrating that not all muscle-specific genes are extinguished by ras. Denervation stimulated DHPR gene expression less than 0.6-fold, despite 8-fold upregulation of delta-subunit mRNA and reciprocal effects on the skeletal and cardiac alpha-actin genes. Thus, DHPR gene induction is prevented by inhibitors of other muscle-specific genes, whereas, at most, relatively small changes in DHPR mRNA abundance occur during adaptation to denervation.

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