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Role of CD14 Expression in the Differentiation-Apoptosis Switch in Human Monocytic Leukemia Cells Treated with 1,25-Dihydroxyvitamin D₃ or Dexamethasone in the Presence of Transforming Growth Factor ß¹

Saitama Cancer Center Research Institute, Ina, Saitama 362-0806 [Y. K., T. K., J. O-K., Y. Y-Y., Y. H.], and Third Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama 359-8513 [Y. K., N. N., K. M.], Japan

Abstract

Transforming growth factor ß (TGF-ß) enhanced the growth-inhibitory activities of dexamethasone (Dex) and 1,25-dihydroxyvitamin D₃ (VD3) on human monocytoid leukemia U937 cells. TGF-ß and VD3 synergistically increased the expression of differentiation-associated markers such as the CD11b and CD14 antigens, whereas TGF-ß and Dex did not. On the other hand, TGF-ß and Dex synergistically increased the number of Apo2.7-positive cells, which represents the early stage of apoptosis, whereas TGF-ß and VD3 did not, suggesting that TGF-ß enhanced apoptosis with Dex and enhanced monocytic differentiation with VD3. In the presence of TGF-ß, the retinoblastoma susceptibility gene product, pRb, was synergistically dephosphorylated by Dex as well as VD3. TGF similarly enhanced the expression of the p21^Waf1 gene in U937 cells treated with Dex and VD3. TGF-ß dose-dependently increased the expression of Bcl-2 and Bad and decreased the expression of Bcl-X_L in U937 cells. Dex enhanced the down-regulation of Bcl-X_L expression in TGF-ß-treated cells, whereas VD3 blocked this down-regulation of Bcl-X_L. However, the down-regulation of Bcl-X_L by treatment with the antisense oligomer did not affect the apoptosis or differentiation of U937 cells. The apoptosis of CD14-positive cells was suppressed in the VD3 plus TGF-ß-treated cultures. These results suggest that the expression of CD14 is involved in the survival of differentiated cells.

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