von Albertini M, Palmetshofer A, Kaczmarek E, Koziak K, Stroka D, Grey S T, Stuhlmeier K M, Robson S C
Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.
Biochem Biophys Res Commun. 1998 Jul 30;248(3):822-9. doi: 10.1006/bbrc.1998.9055.
Inflammation within the vasculature is associated with endothelial cell (EC) perturbation, loss of vascular ATP-diphosphohydrolase activity, and platelet microthrombus formation with release of ATP and ADP into the micro-environment. The nature and effects of purinergic stimulation of EC under these circumstances remain largely undetermined. ATP and ADP activated EC transcribed mRNA from certain transcription factor NF-kappa B target genes and expressed E-selectin protein on cell membranes. Band shift analysis and reporter assays confirmed the activation of NF-kappa B in response to both ATP and ADP. Apoptosis was shown to occur in response to purinergic signaling, potentially through the activation of P2z/P2x7 receptors. Induction of EC activation responses and apoptosis in response to stimulation with ATP and ADP is associated with activation of NF-kappa B.
血管内的炎症与内皮细胞(EC)紊乱、血管ATP二磷酸水解酶活性丧失以及血小板微血栓形成有关,同时ATP和ADP会释放到微环境中。在这种情况下,嘌呤能刺激内皮细胞的性质和影响仍 largely未确定。ATP和ADP激活内皮细胞,使其转录某些转录因子NF-κB靶基因的mRNA,并在细胞膜上表达E-选择素蛋白。凝胶迁移分析和报告基因检测证实,ATP和ADP均可激活NF-κB。研究表明,嘌呤能信号传导可能通过激活P2z/P2x7受体诱导细胞凋亡。内皮细胞激活反应和ATP及ADP刺激诱导的细胞凋亡与NF-κB的激活有关。