Stehlik C, de Martin R, Binder B R, Lipp J
Department of Vascular Biology and Thrombosis Research, VIRCC/University of Vienna, Austria.
Biochem Biophys Res Commun. 1998 Feb 24;243(3):827-32. doi: 10.1006/bbrc.1998.8185.
The inhibitor of apoptosis (iap) proteins belong to a gene family that protect certain cell to undergo programmed cell death in response to a variety of stimuli. By differential screening we have identified a cDNA clone, designated piap, in porcine aortic endothelial cells (PAEC) that turned out by sequence comparison to be a porcine member of the iap family. The expression of piap is strongly up-regulated upon treatment of endothelial cells (EC) with inflammatory cytokines TNF-alpha, IL-1 beta, and LPS. In EC these stimuli lead to the activation of nuclear transcription factor kappa B (NF-kappa B) that plays a role in countering TNF-alpha induced apoptosis. We demonstrate that adenovirus mediated overexpression of I kappa B alpha, an inhibitor of NF-kappa B suppresses the expression of piap in response to TNF-alpha suggesting that piap is one of the NF-kappa B regulated genes that operates to prevent programmed cell death of EC in inflammation.
凋亡抑制蛋白（IAP）属于一个基因家族，可保护特定细胞在多种刺激下发生程序性细胞死亡。通过差异筛选，我们在猪主动脉内皮细胞（PAEC）中鉴定出一个cDNA克隆，命名为piap，经序列比较发现它是IAP家族的猪成员。在用炎性细胞因子TNF-α、IL-1β和LPS处理内皮细胞（EC）后，piap的表达强烈上调。在EC中，这些刺激导致核转录因子κB（NF-κB）活化，NF-κB在对抗TNF-α诱导的凋亡中起作用。我们证明，腺病毒介导的NF-κB抑制剂IκBα的过表达可抑制piap在TNF-α刺激下的表达，这表明piap是NF-κB调控的基因之一，其作用是防止炎症中EC的程序性细胞死亡。
