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Induction of transforming growth factor beta 1 tgf beta 1 receptor expression and tgf beta 1 protein production in retinoic acid treated hl 60 cells possible tgf beta 1 mediated autocrine inhibition



Induction of transforming growth factor beta 1 tgf beta 1 receptor expression and tgf beta 1 protein production in retinoic acid treated hl 60 cells possible tgf beta 1 mediated autocrine inhibition



Blood 77(6): 1248-1255



Treatment of HL-60 cells, a human promyelocytic leukemia cell line, with the vitamin A derivative retinoic acid (RA) for 7 days resulted in a dose-dependent decrease in proliferation and increase in granulocytic differentiation. The role of transforming growth factor-.beta.1 (TGF-.beta.1), a protein with pleiotropic effects on the proliferation and differentiation of various cell types, was examined during RA-induced differentiation of HL-60 cells. Although TGF-.beta.1 alone had little effect on proliferation or differentiation of HL-60 cells, addition of TGF-.beta.1, to HL-60 cells treated with a suboptimum concentration of RA (1.0 nmol/L) resulted in a marked decrease in proliferation with no effect on granulocytic differentiation. Studies of the mechanism of RA-induced TGF-.beta. sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-.beta.1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Maximum induction was achieved after treatment with 10 nmol/LRA and consisted predominantly of the 65-Kd TGF-.beta.1 receptor type. Moreover, RA treatment also resulted in a dose-dependent increase in both TGF-.beta.1 steady-state mRNA expression and production of active TGF-.beta. with maximum induction at 10 nmol/RA. RA treatment of HL-60 cells had no effect on TGF-.beta.2 and TGF-.beta.3 mRNA expression. These data suggest that the effects of RA may be mediated by a TGF-.beta.1-mediated autocrine antiproliferative loop during differentiation of HL-60 cells.

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Accession: 007451898

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PMID: 1848114


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