Sato Y, Teruyama K, Nakano T, Oda N, Abe M, Tanaka K, Iwasaka-Yagi C
Department of Vascular Biology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Ann N Y Acad Sci. 2001 Dec;947:117-23.
Angiogenesis is a complex phenomenon that requires at least migration, proliferation, and tubular morphogenesis of endothelial cells (ECs). Some genes are expressed in ECs during these processes, and therefore the regulation of gene expression in ECs is critical. Increasing evidence suggests that the Ets family of transcription factors plays an important role in angiogenesis. We observed that Ets-1, a prototype of the Ets family of transcription factors, promoted angiogenesis by inducing the expression of matrix metalloproteinases and integrin beta3 in ECs, and the elimination of the transactivation activity of Ets-1 by a dominant negative molecule inhibited angiogenesis. Apoptosis, a term used to describe the terminal morphological and biochemical events seen in programmed cell death, is critical for the development or reconstitution of multicellular organs. Apoptosis of ECs is observed at the initiation of angiogenesis, at the branching or communication with newly formed vessels, and at the regression of neo-vessels. The Ets family of transcription factors is generally thought to be anti-apoptotic. However, there are conflicting reports on the role of Ets-1 in apoptosis. We examined the role of Ets-1 in apoptosis of ECs and found that Ets-1 was pro-apoptotic to ECs by modulating the expression of several apoptosis-related genes.
血管生成是一种复杂的现象，至少需要内皮细胞（ECs）的迁移、增殖和管状形态发生。在这些过程中，一些基因在ECs中表达，因此ECs中基因表达的调控至关重要。越来越多的证据表明，Ets转录因子家族在血管生成中起重要作用。我们观察到，Ets转录因子家族的原型Ets-1通过诱导ECs中基质金属蛋白酶和整合素β3的表达促进血管生成，而一种显性负性分子消除Ets-1的反式激活活性则抑制血管生成。凋亡是一个用于描述程序性细胞死亡中终末形态和生化事件的术语，对多细胞器官的发育或重建至关重要。在血管生成开始时、与新形成血管的分支或连通处以及新生血管的消退过程中，均可观察到ECs的凋亡。一般认为Ets转录因子家族具有抗凋亡作用。然而，关于Ets-1在凋亡中的作用存在相互矛盾的报道。我们研究了Ets-1在ECs凋亡中的作用，发现Ets-1通过调节几个凋亡相关基因的表达对ECs具有促凋亡作用。
