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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Antiapoptotic activities of bcl-2 correlate with vascular maturation and transcriptional modulation of human endothelial cells.
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Antiapoptotic activities of bcl-2 correlate with vascular maturation and transcriptional modulation of human endothelial cells.

机译：bcl-2的抗凋亡活性与人类内皮细胞的血管成熟和转录调控有关。

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摘要

Overexpression of a caspase-resistant form of Bcl-2 (D34A) in human umbilical vein endothelial cells (ECs) implanted into immunodeficient mice promotes the maturation of human EC-lined microvessels invested by vascular smooth muscle cells (VSMCs) of mouse origin. In contrast, EC implants not overexpressing Bcl-2 form only simple, uncoated EC tubes. Here the authors compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of EC expressing different forms of Bcl-2. Wild-type Bcl-2, like the caspase-resistant D34A Bcl-2 mutant, is antiapoptotic in vitro and promotes VSMC recruitment in vivo, whereas a G145E mutant that has diminished antiapoptotic activity in vitro does not promote vessel maturation in vivo. The D34A and wild-type forms of Bcl-2, but not the G145E mutant form of Bcl-2, significantly regulate RNA transcripts previously associated with EC-VSMC interactions and VSMC biology, including matrix Gla protein, insulin-like growth factor-binding protein (IGFBP)-2, matrix metalloproteinase (MMP)-14, ADAM17, stanniocalcin-1, and targets of the nuclear factor (NF)-kappa B, cAMP response element-binding (CREB), and activator protein 1 (AP1) transcription factor families. These effects of Bcl-2 on the transcriptome are detected in ECs cultured as angiogenic three-dimensional (3-D) tubes but are attenuated in ECs cultured as 2-D monolayers. Bcl-2-regulated transcription in ECs may contribute to vascular maturation, and support design of tissue engineering strategies using EC.
机译：植入免疫缺陷小鼠的人脐静脉内皮细胞（EC）中半胱天冬酶抗性形式的Bcl-2（D34A）过表达促进了由小鼠来源的血管平滑肌细胞（VSMC）投资的人EC内衬微血管的成熟。相反，没有过表达Bcl-2的EC植入物仅形成简单的未涂覆EC管。在这里，作者比较了表达不同形式的Bcl-2的EC的体内形成的血管表型和体外的转录组。野生型Bcl-2与耐caspase的D34A Bcl-2突变体一样，在体外具有抗凋亡作用，并在体内促进VSMC募集，而在体外具有减弱的抗凋亡活性的G145E突变体，则不能促进体内血管成熟。 Bcl-2的D34A和野生型形式，而不是Bcl-2的G145E突变体形式，显着调节先前与EC-VSMC相互作用和VSMC生物学相关的RNA转录物，包括基质Gla蛋白，胰岛素样生长因子结合蛋白（IGFBP）-2，基质金属蛋白酶（MMP）-14，ADAM17，斯坦钙蛋白-1和核因子（NF）-κB，cAMP反应元件结合（CREB）和激活蛋白1（AP1）的靶标转录因子家族。 Bcl-2对转录组的这些作用在以血管生成三维（3-D）管培养的EC中被检测到，但在以2-D单层培养的EC中被减弱。 EC中Bcl-2调节的转录可能有助于血管成熟，并支持使用EC进行组织工程策略的设计。

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