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Mitogenesis in fetal rat bone cells simultaneously exposed to type beta transforming growth factor and other growth regulators.

作者信息

Centrella M, McCarthy T L, Canalis E

机构信息

Department of Medicine, Saint Francis Hospital, Hartford, Connecticut 06105.

出版信息

FASEB J. 1987 Oct;1(4):312-7. doi: 10.1096/fasebj.1.4.3498658.

DOI:10.1096/fasebj.1.4.3498658
PMID:3498658
Abstract

Type beta transforming growth factor (TGF-beta) is found in large amounts in bone tissue, and is a potent mitogen for osteoblast-enriched cell cultures obtained from fetal rat parietal bone. Because other local and systemic factors may be presented to bone cells simultaneously with TGF-beta, it is important to understand the effects of this complex growth regulator in such circumstances. Unlike the effects observed in many tissue systems, TGF-beta does not invariably inhibit the mitogenic response of bone cells to other growth promoters. In contrast, other factors such as epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and type alpha tumor necrosis factor (TNF-alpha) limit the response of osteoblastic bone cells to TGF-beta. TGF-beta is a much weaker mitogen for fibroblastic cells obtained from fetal rat bone, whereas fetal bovine serum, EGF, bFGF, and TNF-alpha are more potent stimulators. In addition, TGF-beta does not significantly impair the response of the fibroblastic bone cells to the other tested agents. These findings reinforce a role of TGF-beta as an anabolic bone growth regulator, and suggest that its function may be modified by other local or systemic agents that can also affect bone cells.

摘要

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