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v-src通过抑制血管细胞黏附分子-1和干细胞因子来干扰脾基质细胞的体外红细胞生成刺激能力。

v-src interferes with the in vitro erythropoietic stimulatory ability of spleen stromal cells through repression of vascular cell adhesion molecule-1 and stem cell factor.

作者信息

Yanai N, Shimizu A, Koguma M, Obinata M

机构信息

Department of Cell Biology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.

出版信息

Exp Hematol. 1996 Jul;24(8):883-7.

PMID:8690046
Abstract

A mouse spleen stromal cell line, MSS62, can create an in vitro erythropoietic microenvironment in which development of erythropoietin-responsive progentor cells is stimulated by cell-cell contact via stem cell factor (SCF)/c-Kit and vascular cell adhesion molecule-1 (VCAM-1)/very late activation antigen-4 (VLA-4) interactions between stromal and erythroid cells. To find out the effect of src on the erythropoietic microenvironment, MSS62 cells were transfected with v-src oncogene, and its effect on erythropoietic stimulatory activity was measured. Transfectants with high v-Src activity showed reduction in erythropoietic stimulatory activity. A decrease in cell-surface VCAM-1 and SCF mRNA was accompanied by high v-Src activity. These results suggest that v-Src interferes with the erythropoietic stimulatory activity of the stromal cells through repression of VCAM-1 and SCF.

摘要

小鼠脾基质细胞系MSS62能够创建一个体外红细胞生成微环境,在该环境中,促红细胞生成素反应性祖细胞的发育通过基质细胞与红系细胞之间的干细胞因子(SCF)/c-Kit以及血管细胞黏附分子-1(VCAM-1)/极晚期活化抗原-4(VLA-4)相互作用,经由细胞间接触而受到刺激。为了探究src对红细胞生成微环境的影响,用v-src癌基因转染MSS62细胞,并检测其对红细胞生成刺激活性的影响。具有高v-Src活性的转染子表现出红细胞生成刺激活性降低。高v-Src活性伴随着细胞表面VCAM-1和SCF mRNA的减少。这些结果表明,v-Src通过抑制VCAM-1和SCF来干扰基质细胞的红细胞生成刺激活性。

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