Sorio C, Melotti P, Dusi S, Berton G
Institute of General Pathology, University of Verona, Italy.
FEBS Lett. 1993 Aug 2;327(3):315-20. doi: 10.1016/0014-5793(93)81012-o.
We investigated modulation of p60src expression in human mononuclear phagocytes. By analysis of [35S]methionine-labelled cells we found that synthesis of p60src is higher in human monocytes compared to macrophages derived from in vitro cultivation of monocytes. Western blot analysis showed that expression of p60src in monocyte-derived macrophages can be enhanced if monocytes are differentiated into macrophages in the presence of interferon-gamma (IFN-gamma), or tumor necrosis factor-alpha (TNF-alpha). Enhanced p60src expression caused by IFN-gamma or TNF-alpha correlated with an enhanced autophosphorylating kinase activity assayed in anti-p60src immune precipitates. In vivo phosphorylation of p60src and analysis of phosphopeptides by tryptic digestion showed that treatment with cytokines did not affect the pattern of phosphorylation of distinct phosphopeptides. The human monocytic cell lines, U937 and HL-60, induced to differentiate along the monocytic pathway by IFN-gamma, or a combination of IFN-gamma and TNF-alpha, expressed higher amounts of the p60src, but not of the p59fyn or p62yes, kinase activity. These findings show that p60src is modulated in the course of differentiation of human monocytes to macrophages, and that macrophage-activating cytokines increase p60src expression in human monocyte-derived macrophages.
我们研究了人类单核吞噬细胞中p60src表达的调节情况。通过对[35S]甲硫氨酸标记的细胞进行分析，我们发现与单核细胞体外培养衍生的巨噬细胞相比，人类单核细胞中p60src的合成更高。蛋白质免疫印迹分析表明，如果单核细胞在干扰素-γ（IFN-γ）或肿瘤坏死因子-α（TNF-α）存在的情况下分化为巨噬细胞，单核细胞衍生的巨噬细胞中p60src的表达会增强。IFN-γ或TNF-α引起的p60src表达增强与在抗p60src免疫沉淀物中检测到的自磷酸化激酶活性增强相关。p60src的体内磷酸化及通过胰蛋白酶消化对磷酸肽的分析表明，细胞因子处理不会影响不同磷酸肽的磷酸化模式。人类单核细胞系U937和HL-60，在IFN-γ或IFN-γ与TNF-α的组合诱导下沿单核细胞途径分化，表达了更高量的p60src激酶活性，但p59fyn或p62yes激酶活性未增加。这些发现表明，p60src在人类单核细胞向巨噬细胞分化过程中受到调节，并且巨噬细胞激活细胞因子会增加人类单核细胞衍生巨噬细胞中p60src的表达。
