Ohneda O, Yanai N, Obinata M
Department of Cell Biology, Tohoku University, Sendai, Japan.
Development. 1992 Jan;114(1):245-52. doi: 10.1242/dev.114.1.245.
Mutations at the murine dominant-white spotting locus (W) (c-kit) affect various aspects of hematopoiesis. We have made antibodies against c-Kit with the synthetic peptides deduced from the murine c-kit gene and examined the role of c-Kit in erythropoiesis. The antibody inhibited the stromal cell-dependent large colony formation of the erythroid progenitors. In the culture of erythropoietin-responsive erythroid progenitors of the anemia-inducing Friend virus-infected mouse spleen, the antibody inhibited only proliferation, but not differentiation of the progenitor cells. The inhibition was effective only at the early phase (within 6 hours after erythropoietin addition) before the cells start to proliferate induced by erythropoietin. During the early phase, erythropoietin down-regulated c-kit gene expression. These results suggest a mechanism of combined action of c-Kit with erythropoietin on the lineage-restricted erythroid progenitor cells.
小鼠显性白斑位点（W）（c-kit）的突变会影响造血的各个方面。我们利用从小鼠c-kit基因推导的合成肽制备了抗c-Kit抗体，并研究了c-Kit在红细胞生成中的作用。该抗体抑制了红细胞祖细胞依赖基质细胞的大集落形成。在诱导贫血的弗氏病毒感染小鼠脾脏中促红细胞生成素反应性红细胞祖细胞的培养中，该抗体仅抑制祖细胞的增殖，而不抑制其分化。这种抑制仅在细胞开始由促红细胞生成素诱导增殖之前的早期阶段（添加促红细胞生成素后6小时内）有效。在早期阶段，促红细胞生成素下调c-kit基因表达。这些结果提示了c-Kit与促红细胞生成素对谱系受限的红细胞祖细胞联合作用的机制。
