College of Veterinary Medicine, Yangzhou University, 12 East Wenhui Road, Yangzhou, 225009, People's Republic of China.
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, 225009, People's Republic of China.
Sci Rep. 2017 Jun 28;7(1):4331. doi: 10.1038/s41598-017-04555-2.
Parthanatos is a newly discovered form of PARP-1-dependent programmed cell death. It has been reported to play an important role in several cancer or tumour cells; however, few studies have been performed in normal cells. Cadmium is a highly toxic pollutant and is reported to induce autophagy and apoptosis in multiple cell types. Although cadmium toxicity induces cell death, the underlying mechanism is not fully understood. Therefore, in this study we aimed to investigate the mechanism of Cadmium -induced cell damage using rat proximal tubular cell line NRK-52E and primary rat proximal tubular (rPT) cells. Our results indicated that parthanatos and the MAPK signalling pathway contribute to Cadmium-induced cell death, and that oxidative stress and mitochondrial damage play key roles in this process. In addition, parthanatos with oxidative stress has a synergistic effect on apoptosis, and JNK1/2 and p38 contribute to parthanatos.
细胞 Parthanatos 是一种新发现的 PARP-1 依赖性程序性细胞死亡形式。据报道，它在几种癌症或肿瘤细胞中发挥着重要作用；然而，在正常细胞中进行的研究较少。镉是一种毒性很强的污染物，据报道可在多种细胞类型中诱导自噬和细胞凋亡。尽管镉毒性会导致细胞死亡，但具体机制尚不完全清楚。因此，在这项研究中，我们旨在使用大鼠近曲小管细胞系 NRK-52E 和原代大鼠近曲小管 (rPT) 细胞来研究镉诱导的细胞损伤的机制。我们的结果表明，细胞 Parthanatos 和 MAPK 信号通路参与了镉诱导的细胞死亡，氧化应激和线粒体损伤在此过程中起关键作用。此外，氧化应激与细胞 Parthanatos 协同促进细胞凋亡，并且 JNK1/2 和 p38 参与细胞 Parthanatos。
