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Transforming growth factor type β1 modulates the effects of basic fibroblast growth factor on growth and phenotypic expression of rat astroblasts in vitro
Author(s) -
Labourdette Gerard,
Janet Thierry,
Laeng Pascal,
Perraud Frederic,
Pettmann Brigitte,
Lawrence David
Publication year - 1990
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041440315
Subject(s) - basic fibroblast growth factor , transforming growth factor , growth factor , epidermal growth factor , biology , dna synthesis , stimulation , endocrinology , medicine , fibroblast growth factor , platelet derived growth factor , platelet derived growth factor receptor , cell growth , in vitro , cell culture , microbiology and biotechnology , receptor , biochemistry , genetics
In a search of the growth factors possibly involved in brain ontogenesis we have examined the effects of transforming growth factor β1 (TGF‐β1) on the growth and phenotypic expression of rat astroblasts in primary culture. Along TGF‐β1 elicited only a slight negative effect on the growth of these cells. However, this factor was found to modulate the mitogenic effects of other growth factors. On quiescent cells it potentiates the mitogenic effect of basic fibroblast growth factor (bFGF) but not that of other growth factors, namely, epidermal growth factor (EGF), platelet‐derived growth factor (PDGF), and thrombin. TGF‐β1 did not modulate significantly the stimulatory effect of these growth factors on the activity of the enzyme glutamine synthetase (GS); but kinetic studies showed that TGF‐β1 delays the stimulation of GS activity. DNA synthesis monitored by the incorporation of [ 125 I]iododeoxyuridine ( 125 I‐dUrd) was maximum after 24–30 h of treatment with bFGF. With bFGF plus TGF‐β1 the maximum was shifted to 30–36 h. This shift is compatible with the idea that TGF‐β1 induces responsiveness in some cells which are otherwise unresponsive to the mitogenic action of bFGF, and that this induction requires some time. This hypothesis is sustained by the observation that in cells treated for only 12 h with bFGF, the treatment with TGF‐β1 for the same 12 h or for longer time did not stimulate significantly the cell growth. Stimulation occurred only when the bFGF treatment was continued after 12 h. Potentiation of the mitogenic effect of bFGF and shift of the maximum 125 I‐dUrd incorporation towards 24 h was seen with cells pretreated with TGF‐β1. This potentiation effect decreased with increasing time between the two treatments. The potentiation effect of TGF‐β1 is not mediated by an induction of new bFGF membrane receptors as seen by binding studies.