Geng Wenqing, Wang Jinglei, Xie Lili, Song Yan, Cao Maohong, Shen Jiabing
Department of Neurology, Affiliated Hospital of Nantong University, 20#, Xisi RD, Nantong, Jiangsu, 226001, People's Republic of China.
Department of Neurology, The People's Hospital of Hai'an, Nantong, Jiangsu, 226600, People's Republic of China.
Neurotox Res. 2022 Apr;40(2):461-472. doi: 10.1007/s12640-022-00483-w. Epub 2022 Feb 22.
Intracerebral hemorrhage (ICH) is a serious condition with a particularly high mortality rate. Gli-similar 2 (Glis2) has been reported to play an important role in the pathogenesis of ICH; however, its underlying mechanisms and biological significance remains unclear. In the present study, a specific interaction between Glis2 and p75, a member of the tumor necrosis factor receptor superfamily, was identified both in vivo and in vitro. These experiments further indicated that p75 may interact with Glis2, and that the complex was transported into the nucleus, initially, inducing neuronal death. Furthermore, the mechanism of neuronal death was explored, and may have been mediated via the activation of the mitochondrial-dependent apoptotic pathway, and this was further investigated in the pathogenesis of ICH in rats in vivo. The study may provide evidences for regulating p75-Glis2 complex as a potential reliable treatment for the secondary damage following ICH.
脑出血（ICH）是一种严重的病症，死亡率特别高。据报道，Gli-similar 2（Glis2）在脑出血的发病机制中起重要作用；然而，其潜在机制和生物学意义仍不清楚。在本研究中，在体内和体外均鉴定出Glis2与肿瘤坏死因子受体超家族成员p75之间的特异性相互作用。这些实验进一步表明，p75可能与Glis2相互作用，并且该复合物被转运到细胞核中，最初会诱导神经元死亡。此外，还探讨了神经元死亡的机制，可能是通过线粒体依赖性凋亡途径的激活介导的，并在大鼠脑出血的体内发病机制中进一步进行了研究。该研究可能为调节p75-Glis2复合物作为脑出血后继发性损伤的潜在可靠治疗方法提供证据。
