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Human Platelet-Derived Transforming Growth Factor-βStimulates Parameters of Bone Growth in Fetal Rat Calvariae^*

Department of Medicine (Endocrine Section) and Research Laboratory, St. Francis Hospital and Medical Center Hartford, Connecticut 06105
The University of Connecticut Health Center Farmington, Connecticut 06032
the Department of Biochemistry, University of Massachusetts Medical Center Worcester, Massachusetts 01605

Address requests for reprints to: Dr. Michael Centrella, Research Laboratory, Saint Francis Hospital and Medical Center, 114 Woodland Street, Hartford, Connecticut 06105.

Abstract

Human platelet-derived transforming growth factor type β (TGFβ) is mitogenic for fetal rat calvariae in serum-free organ culture. It enhances DNA synthesis in short (24-h) and long (48- to 96-h) term cultures, but produces no significant stimulatory effects on bone collagen synthesis or alkaline phosphatase activity (two parameters of differentiated osteoblastic cell-type function) when present continuously in culture. Transitory treatment with TGFβ, however, induces a subsequent stimulation of collagen and noncollagen protein synthesis that depends on prior cell replication, suggesting an increase in the number of newly differentiated bone cells. In addition, TGFβ increases prostaglandin release, but this effect is probably unrelated to its mitogenic function. TGFβ activity is also found in culture medium conditioned by fetal rat calvariae, and the bone-derived factor produces effects similar to those of the human platelet factor. This polypeptide, therefore, may have an important function in early stages of bone development as well as bone repair after trauma-induced platelet degranulation. (Endocrinology 119: 2306–2312, 1986)

Footnotes

^* Presented in part at the 25th Annual Meeting of the American Society for Cell Biology, Atlanta, GA, November 1985. This work was supported by NIADDK Grant AM-21707 and NCI Grant CA-34610.

Received April 29, 1986.

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