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Insulin increases the steady state level of alpha-1(I) procollagen mRNA in the osteoblast-rich segment of fetal rat calvaria.

作者信息

Craig R G, Rowe D W, Petersen D N, Kream B E

机构信息

Department of BioStructure and Function, University of Connecticut Health Center, Farmington 06032.

出版信息

Endocrinology. 1989 Sep;125(3):1430-7. doi: 10.1210/endo-125-3-1430.

Abstract

Insulin at 3-100 nM increased the steady state level of alpha-1(I) procollagen mRNA and stimulated collagen synthesis in the osteoblast-rich segment of central bone from 21-day-old fetal rat calvaria. The increases in the level of procollagen mRNA and the rate of collagen synthesis were observed 18 h after the addition of insulin to the cultures. The removal of insulin from calvaria incubated for 24 h with 3 nM insulin caused collagen synthesis and the level of alpha-1(I) procollagen mRNA to return to control values within 5 h. Adding insulin back to calvaria withdrawn from insulin treatment for 3 h did not rescue the decay in collagen synthesis or the level of alpha-1(I) procollagen mRNA. Insulin increased the steady state levels of alpha-1(I) procollagen mRNA in the presence of the RNA synthesis inhibitor actinomycin-D. Our data suggest that in fetal rat bone, one mechanism by which insulin increases the steady state level of alpha-1(I) procollagen mRNA may be by altering its stability.

摘要

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