MONOCYTE DIFFERENTIATION-- ROLE OF TYROSINE PHOSPHORYLATION VIA CSF-1 RECEPTOR

用c-fms转染小鼠造血细胞系32 D， CSF-I受体，一种酪氨酸激酶（TK）的抑制剂。 在没有 在CSF-1中，转染细胞显示中等水平的花生四烯酸 （A.A.）释放并产生大量的前列腺素E2 （PGE 2）与原始细胞系相比。 暴露 转染细胞的CSF-1，同时诱导大量增加， 花生四烯酸的释放，然而，导致抑制PGE 2 生产 向细胞中添加酪氨酸激酶抑制剂ST 638 在CSF-1缺失的情况下，转染c-fms可在10 到60分钟。 在CSF-1存在的情况下将其添加到相同的细胞中， 受体可调节环氧合酶活性。 的不同影响 在存在或不存在CSF-1的情况下PGE 2产生的CSF-1受体 酪氨酸激酶抑制剂对PGE 2的相反作用表明， 无论是受体本身还是受体-配体复合物， 活性的，但不同的，通过酪氨酸磷酸化的信号。

The mouse hematopoietic cell ine, 32D, was transfected with c-fms, which enclodes for the CSF-1 receptor, a tyrosine kinase (TK). In the absence of CSF-1, transfected cells show moderate levels of arachidonic acid (A.A.) release and produce a substantial amount of prostaglandin E2 (PGE2) in comparison with the original cell line. Exposure of transfected cells to CSF-1, while inducing a substantial increase in arachidonate release, nevertheless resulted in inhibition of PGE2 production. Addition of ST638, a tyrosine kinase inhibitor, to cells transfected with c-fms in the absense of CSF-1 inhibited PGE2 within 10 to 60 minutes. Its addtion to the same cells in the presence of CSF-1 receptor may regulate cyclooxygenase activity. The different effect of CSF-1 receptor of PGE2 production in the presence or absence of CSF-1 and the opposite effect of a tyrosine kinase inhibitor on PGE2 suggest that both the receptor alone or the receptor-ligand complex transduce on active, but different, signal through tyrosine phosphorylation.