Rajesh Mohanraj, Mukhopadhyay Partha, Bátkai Sándor, Godlewski Grzegorz, Haskó György, Liaudet Lucas, Pacher Pál
Section On Oxidative Stress Tissue Injury, Laboratory of Physiological Studies, NIAAA, National Institutes of Health, 5625 Fishers Lane, MSC-9413, Bethesda, MD 20892-9413, USA.
Biochem Biophys Res Commun. 2006 Nov 17;350(2):352-7. doi: 10.1016/j.bbrc.2006.09.049. Epub 2006 Sep 20.
Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which plays an important role in regulating cell death and cellular responses to DNA repair. Pharmacological inhibitors of PARP are being considered as treatment for cancer both in monotherapy as well as in combination with chemotherapeutic agents and radiation, and were also reported to be protective against untoward effects exerted by certain anticancer drugs. Here we show that pharmacological inhibition of PARP with 3-aminobenzamide or PJ-34 dose-dependently reduces VEGF-induced proliferation, migration, and tube formation of human umbilical vein endothelial cells in vitro. These results suggest that treatment with PARP inhibitors may exert additional benefits in various cancers and retinopathies by decreasing angiogenesis.
聚(ADP-核糖)聚合酶(PARP)是一种核酶,在调节细胞死亡和细胞对DNA修复的反应中起重要作用。PARP的药理抑制剂正在被考虑用于癌症治疗,无论是单一疗法还是与化疗药物及放疗联合使用,并且据报道还能预防某些抗癌药物产生的不良影响。在这里,我们表明用3-氨基苯甲酰胺或PJ-34对PARP进行药理抑制可剂量依赖性地降低体外人脐静脉内皮细胞中VEGF诱导的增殖、迁移和管腔形成。这些结果表明,PARP抑制剂治疗可能通过减少血管生成在各种癌症和视网膜病变中发挥额外的益处。