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首页> 外文期刊>Journal of Cellular Physiology >ETS-1 converts endothelial cells to the angiogenic phenotype by inducing the expression of matrix metalloproteinases and integrin beta3.
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ETS-1 converts endothelial cells to the angiogenic phenotype by inducing the expression of matrix metalloproteinases and integrin beta3.

机译:ETS-1转换内皮细胞血管生成表型的诱导矩阵的表达式金属蛋白酶和整合素beta3。

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摘要

The transcription factor ETS-1 is induced in endothelial cells (ECs) by angiogenic growth factors and the specific elimination of ETS-1 synthesis by antisense oligodeoxynucleotide inhibited angiogenesis in vitro (Iwasaka et al., 1996, J Cell Physiol 169:522-531). To understand the precise role of ETS-1 in angiogenesis, we established both high and low ETS-1 expression EC lines and compared angiogenic properties of these cell lines with those of the parental murine EC line, MSS-31. Although growth rate was almost identical for each cell line, the invasiveness was markedly enhanced in high ETS-1 expression cells and reduced in low ETS-1 expression cells compared with that of parental cells. The gene expressions of matrix metalloproteinases (MMP-1, MMP-3, and MMP-9) and gelatinolytic activity of MMP-9 were significantly increased in high ETS-1 expression cells. Low ETS-1 expression cells could not spread on a vitronectin substratum, and the phosphorylation of focal adhesion kinase was markedly impaired because of the reduced expression of integrin beta3. These results indicate that ETS-1 is a principal regulator that converts ECs to the angiogenic phenotype.
机译:的转录因子ETS-1诱导内皮细胞血管生成(ECs)的增长因素和特定的消除ETS-1合成的反义oligodeoxynucleotide体外抑制血管生成(Iwasaka et al .,1996年,J细胞杂志169:522 - 531)。精确ETS-1在血管生成中的作用,我们建立了高和低ETS-1 EC表达线和比较这些血管生成属性与亲代小鼠EC的细胞系线,MSS-31。对于每一个细胞系,侵袭性相同ETS-1表达显著增强在高细胞和减少低ETS-1表达细胞相比与亲代细胞。基质金属蛋白酶的表达(金属蛋白酶- 1,MMP-3和MMP-9)和gelatinolytic活动MMP-9在高ETS-1显著增加表达的细胞。不能传播vitronectin根基,粘着斑激酶的磷酸化明显受损,因为减少了整合素的表达beta3。表明ETS-1主要监管机构血管生成表型转换ECs。

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