Stroka D M, Badrichani A Z, Bach F H, Ferran C
Immunobiology Research Center, Beth Israel-Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Blood. 1999 Jun 1;93(11):3803-10.
A1 is an anti-apoptotic bcl gene that is expressed in endothelial cells (EC) in response to pro-inflammatory stimuli. We show that in addition to protecting EC from apoptosis, A1 inhibits EC activation and its associated expression of pro-inflammatory proteins by inhibiting the transcription factor nuclear factor (NF)-kappaB. This new anti-inflammatory function gives a broader dimension to the protective role of A1 in EC. We also show that activation of NF-kappaB is essential for the expression of A1. Taken together, our data suggest that A1 downregulates not only the pro-apoptotic and pro-inflammatory response, but also its own expression, thus restoring a quiescent phenotype to EC.
A1是一种抗凋亡的bcl基因，在内皮细胞（EC）中，它会响应促炎刺激而表达。我们发现，除了保护内皮细胞免于凋亡外，A1还通过抑制转录因子核因子（NF）-κB来抑制内皮细胞的激活及其相关的促炎蛋白表达。这种新的抗炎功能为A1在内皮细胞中的保护作用赋予了更广泛的意义。我们还表明，NF-κB的激活对于A1的表达至关重要。综上所述，我们的数据表明，A1不仅下调促凋亡和促炎反应，还下调其自身的表达，从而使内皮细胞恢复静止表型。
