Growth Inhibitor from BSC-1 Cells Closely Related to Platelet Type β Transforming Growth Factor

Tucker, Ronald F.; Shipley, Gary D.; Moses, Harold L.; Holley, Robert W.

doi:10.1126/science.6093254

Cited by 707 publications

(302 citation statements)

References 12 publications

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“…For example, TGF-/$1 does not directly stimulate DNA synthesis in adherent, G0-synchmnized fibroblasts, and it can even inhibit the proliferation mediated by mitogens such as serum and EGF (Massagu6, 1990;Moses et al, 1990;Sporn and Roberts, 1990). TGF-~I is also unusual in its ability to stimulate anchorage-independent growth of certain fibroblastic cell lines (Roberts et al, 1981;Assoian et al, 1983;Moses et al, 1985;Tucker et al, 1984). These distinct cellular effects of TGF-/$1 are consistent with recent studies showing that the TGF-/31 receptor has a serine/threonine kinase activity rather than the tyrosine kinase activity typically associated with peptlde growth factor receptors (Linet al, 1992;Massagu6, 1992).…”

Section: Ell Cycle Progression In Nontransformed Fibroblastssupporting

confidence: 76%

A cell cycle and mutational analysis of anchorage-independent growth: cell adhesion and TGF-beta 1 control G1/S transit specifically

Han

Guadagno

Dalton

et al. 1993

The Journal of Cell Biology

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Abstract. We have examined cell cycle control of anchorage-independent growth in nontransformed fibroblasts. In previous studies using Go-synchronized NRK and NIH-3T3 cells, we showed that anchorageindependent growth is regulated by an attachmentdependent transition at G1/S that resembles the START control point in the cell cycle of Saccharomyces cerevisiae. In the studies reported here, we have synchronized NRK and NIH-3T3 fibroblasts immediately after this attachment-dependent transition to determine if other portions of the fibroblast cell cycle are similarly regulated by adhesion. Our results show that S-, G2-, and M-phase progression proceed in the absence of attachment. Thus, we conclude that the adhesion requirement for proliferation of these cells can be explained in terms of the single START-like transition. In related studies, we show that TGF-/~I overrides the attachment-dependent transition in NRK and AKR-2B fibroblasts (lines in which TGF-/$1 induces anchorageindependent growth), but not in NIH-3T3 or Balb/c 3T3 fibroblasts (lines in which TGF-/31 fails to induce anchorage-independent growth). These results show that (a) adhesion and TGF-/31 can have similar effects in stimulating cell cycle progression from G1 to S and (b) the differential effects of TGF-fll on anchorageindependent growth of various fibroblast lines are directly reflected in the differential effects of the growth factor at G1/S. Finally, we have randomly mutagenized NRK fibroblasts to generate mutant lines that have lost their attachment/TGF-~l requirement for G1/S transit while retaining their normal mitogen requirements for proliferation. These clones, which readily proliferate in mitogen-supplemented soft agar, appear non-transformed in monolayer: they are well spread, nonrefractile, and contact inhibited. The existence of this new fibroblast phenotype demonstrates (a) that the growth factor and adhesion/TGF-~/1 requirements for cell cycle progression are genetically separable, (b) that the two major control points in the fibroblast cell cycle (G0/G1 and G1/S) are regulated by distinct extracellular signals, and (c) that the genes regulating anchorage-independent growth need not be involved in regulating contact inhibition, focus formation, or growth factor dependence.

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Section: Ell Cycle Progression In Nontransformed Fibroblastssupporting

confidence: 76%

A cell cycle and mutational analysis of anchorage-independent growth: cell adhesion and TGF-beta 1 control G1/S transit specifically

Han

Guadagno

Dalton

et al. 1993

The Journal of Cell Biology

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“…Skeletal TGF-,1 was determined by the mink lung cell bioassay (18,19) and by specific enzyme-linked immunosorbend assays (ELISA) for TGF-fi1 and TGF-f32. For total TGF-,6 bioactivity quantification, mink lung cells (MvlLu, CCL64; American Type Culture Collection, Rockville, MD) were suspended in MEM medium supplemented with 10% FCS (GIBCO, Eggenstein, Germany), plated at 6000 cell/well in 96-well plates and allowed to attach for 4 h. The medium was then aspirated and replaced with serum-free MEM containing bone matrix extracts at a dilution of 1:100 or serial dilutions of TGF-# 1 purified from human platelets (R&D Systems, Minneapolis, MN).…”

Section: Tgf-f3 Measurementsmentioning

confidence: 99%

Parathyroid hormone increases the concentration of insulin-like growth factor-I and transforming growth factor beta 1 in rat bone.

Laukhuf²,

et al. 1995

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Intermittent treatment with parathyroid hormone (PTH) increases bone mass in experimental animals and humans. In vitro studies have suggested that the anabolic effect of PTH may be mediated by local growth factors. However, the relevance of these findings to in vivo situations remains unclear. In this study, we examined a time course of daily s.c. injections of hPTH(1-34) on the skeletal concentration of insulin-like growth factor (IGF)-I, IGF-II, and transforming growth factor (TGF-.3) in the proximal tail vertebrae of male rats. PTH caused a time and dose-dependent increase in the bone mineral density of the lumbar spine. This anabolic effect on bone mass was accompanied by progressive increases in bone matrix-associated IGF-I and TGF-fl1. Increases in IGF-I and TGF-1i1 became apparent after four and eight weeks of PTH treatment respectively and persisted through week 12. PTH had no effect on circulating IGF-I, suggesting that the increase of bone matrix IGF-I was due to the local effect of PTH on bone tissue directly rather than to an increase of circulating IGF-I. These data are consistent with the hypothesis that IGF-I and TGF-f81 may play a role as local mediators of the anabolic effects of PTH on bone metabolism. (J. Clin. Invest. 1995. 96:767-774.)

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“…In this regard, TGF-I3 and a growth inhibitor from green monkey kidney cells (BSC-1) have been shown to have nearly identical biologic activity, and to compete for binding to the same membrane receptor (13,34). The BSC-1 cells produce the inhibitor when arrested at saturation density.…”

Section: Shows the I N D U C T I O N O F Tgf-/3 M R N A In T Cells Atmentioning

confidence: 99%

Production of transforming growth factor beta by human T lymphocytes and its potential role in the regulation of T cell growth.

Kehrl¹,

Wakefield²,

Roberts³

et al. 1986

The Journal of Experimental Medicine

1,482

615

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This study examines the potential role of transforming growth factor beta (TGF-beta) in the regulation of human T lymphocyte proliferation, and proposes that TGF-beta is an important autoregulatory lymphokine that limits T lymphocyte clonal expansion, and that TGF-beta production by T lymphocytes is important in T cell interactions with other cell types. TGF-beta was shown to inhibit IL-2-dependent T cell proliferation. The addition of picograms amounts of TGF-beta to cultures of IL-2-stimulated human T lymphocytes suppressed DNA synthesis by 60-80%. A potential mechanism of this inhibition was found. TGF-beta inhibited IL-2-induced upregulation of the IL-2 and transferrin receptors. Specific high-affinity receptors for TGF-beta were found both on resting and activated T cells. Cellular activation was shown to result in a five- to sixfold increase in the number of TGF-beta receptors on a per cell basis, without a change in the affinity of the receptor. Finally, the observations that activated T cells produce TGF-beta mRNA and that TGF-beta biologic activity is present in supernatants conditioned by activated T cells is strong evidence that T cells themselves are a source of TGF-beta. Resting T cells were found to have low to undetectable levels of TGF-beta mRNA, while PHA activation resulted in a rapid increase in TGF-beta mRNA levels (within 2 h). Both T4 and T8 lymphocytes were found to make mRNA for TGF-beta upon activation. Using both a soft agar assay and a competitive binding assay, TGF-beta biologic activity was found in supernatants conditioned by T cells; T cell activation resulted in a 10-50-fold increase in TGF-beta production. Thus, TGF-beta may be an important antigen-nonspecific regulator of human T cell proliferation, and important in T cell interaction with other cell types whose cellular functions are modulated by TGF-beta.

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Growth Inhibitor from BSC-1 Cells Closely Related to Platelet Type β Transforming Growth Factor

Cited by 707 publications

References 12 publications

A cell cycle and mutational analysis of anchorage-independent growth: cell adhesion and TGF-beta 1 control G1/S transit specifically

A cell cycle and mutational analysis of anchorage-independent growth: cell adhesion and TGF-beta 1 control G1/S transit specifically

Parathyroid hormone increases the concentration of insulin-like growth factor-I and transforming growth factor beta 1 in rat bone.

Production of transforming growth factor beta by human T lymphocytes and its potential role in the regulation of T cell growth.

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