TY - JOUR
T1 - Transforming growth factor type β can act as a potent competence factor for AKR-2B cells
AU - Goustin, Anton Scott
AU - Nuttall, Greg A.
AU - Leof, Edward B.
AU - Ranganathan, Gouri
AU - Moses, Harold L.
PY - 1987/10
Y1 - 1987/10
N2 - Transforming growth factor type β (TGFβ) is a pleiotropic regulator of cell growth with specific high-affinity cell-surface receptors on a large number of cells; its mechanism of action, however, is poorly defined. In this report, we utilized the mouse fibroblast line AKR-2B to explore the question of the temporal requirements during the cell cycle in regard to both the growth inhibitory and the growth stimulatory action of TGFβ. The results indicate that AKR-2B cells are most sensitive to the inhibitory action of TGFβ during early to mid-G1. In addition, TGFβ need be present only briefly (as little as l min) in order to exert its inhibitory effect on EGF-induced DNA synthesis. Likewise, the stimulatory effect of TGFβ in the absence of EGF requires only an equally brief exposure to TGFβ. Use of homogeneous 125I-labeled TGFβ in a cell-binding assay demonstrates that TGFβ bound to cell-surface receptors can readily exchange into the culture medium T 1 2 = 120 min), helping to rule out the possibility that persistent receptor-bound TGFβ is the source of a continuous stimulus. The data indicate that TGFβ exposure induces a stable state in the cell (T 1 2 = 20 h) similar to but distinct from the state of "competence" induced by platelet-derived growth factor (PDGF).
AB - Transforming growth factor type β (TGFβ) is a pleiotropic regulator of cell growth with specific high-affinity cell-surface receptors on a large number of cells; its mechanism of action, however, is poorly defined. In this report, we utilized the mouse fibroblast line AKR-2B to explore the question of the temporal requirements during the cell cycle in regard to both the growth inhibitory and the growth stimulatory action of TGFβ. The results indicate that AKR-2B cells are most sensitive to the inhibitory action of TGFβ during early to mid-G1. In addition, TGFβ need be present only briefly (as little as l min) in order to exert its inhibitory effect on EGF-induced DNA synthesis. Likewise, the stimulatory effect of TGFβ in the absence of EGF requires only an equally brief exposure to TGFβ. Use of homogeneous 125I-labeled TGFβ in a cell-binding assay demonstrates that TGFβ bound to cell-surface receptors can readily exchange into the culture medium T 1 2 = 120 min), helping to rule out the possibility that persistent receptor-bound TGFβ is the source of a continuous stimulus. The data indicate that TGFβ exposure induces a stable state in the cell (T 1 2 = 20 h) similar to but distinct from the state of "competence" induced by platelet-derived growth factor (PDGF).
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U2 - 10.1016/0014-4827(87)90388-0
DO - 10.1016/0014-4827(87)90388-0
M3 - Article
C2 - 2888675
AN - SCOPUS:0023607855
SN - 0014-4827
VL - 172
SP - 293
EP - 303
JO - Experimental Cell Research
JF - Experimental Cell Research
IS - 2
ER -