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K Uchimaru

Publications and source records attributed to K Uchimaru.

20 records · Page 2Linked to original sources

Bone marrow stromal cells produce and respond to activin A: interactions with basic fibroblast growth factor and platelet-derived growth factor.

Activin A, a homodimer of the beta A-chain, regulates hematopoiesis. We recently reported that murine bone marrow (BM) stromal cells, ST2 and MC3T3-G2/PA6, produce activin A [16]. Basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF), potent mitogens of BM stromal cells, induced a rapid increase in beta A-chain mRNA levels and activin secretion in these cells. Cycloheximide (CHX) did not inhibit the increases in beta A-chain mRNA levels, suggesting that these growth factors directly stimulate beta A-chain gene expression. Furthermore, activin A stimulated mitogenesis in ST2 cells, by itself and with bFGF and PDGF. Consistent with this observation, we detected mRNAs of activin A receptors in the murine stromal cells. These findings suggest that BM stromal cells, stimulated by bFGF and PDGF, produce activin A, which may stimulate stromal cells themselves in concert with these peptide growth factors.

Activin Receptors↗

Tumor necrosis factor and interleukin-1 induce activin A gene expression in a human bone marrow stromal cell line.

Activin A, a homodimer of the beta A chain, regulates hematopoiesis. In a human bone marrow-derived stromal cell line, KM-102, phorbol myristate acetate, tumor necrosis factor-alpha and interleukin-1 beta induced great increases in beta A chain mRNA levels and production of activin A activities. The phorbol ester-induced beta A chain gene expression was inhibited by cycloheximide and down regulation of protein kinase C, whereas the cytokine-induced expression was little affected by these treatments. These results indicate that the inflammatory cytokines directly stimulate beta A chain gene expression via protein kinase C-independent pathways.

Activins↗