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bcl-2基因可防止碱性成纤维细胞生长因子缺乏的小鼠主动脉内皮细胞发生凋亡。

bcl-2 gene prevents apoptosis of basic fibroblast growth factor-deprived murine aortic endothelial cells.

作者信息

Kondo S, Yin D, Aoki T, Takahashi J A, Morimura T, Takeuchi J

机构信息

Department of Neurosurgery, National Utano Hospital, Kyoto, Japan.

出版信息

Exp Cell Res. 1994 Aug;213(2):428-32. doi: 10.1006/excr.1994.1219.

Abstract

Growth factors such as basic fibroblast growth factor (bFGF) have been found to promote the survival and proliferation of endothelial cells. However, the mechanism by which growth factors control the regeneration and degeneration of the endothelial cells remained poorly understood. In this study, we demonstrated that apoptosis of murine aortic endothelial (MAE) cells was induced by deprivation of bFGF but required new RNA and protein synthesis. Furthermore, enforced expression of bcl-2 gene in MAE cells using gene transfer techniques decreased apoptosis induced by deprivation of bFGF. These findings suggest that bcl-2 interferes with a pathway for endothelial cell death that is induced by deprivation of bFGF.

摘要

诸如碱性成纤维细胞生长因子(bFGF)等生长因子已被发现可促进内皮细胞的存活和增殖。然而,生长因子控制内皮细胞再生和退化的机制仍知之甚少。在本研究中,我们证明,去除bFGF可诱导小鼠主动脉内皮(MAE)细胞凋亡,但这需要新的RNA和蛋白质合成。此外,利用基因转移技术在MAE细胞中强制表达bcl-2基因可减少因去除bFGF而诱导的细胞凋亡。这些发现表明,bcl-2可干扰因去除bFGF而诱导的内皮细胞死亡途径。

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