P75NTR Interacts with the Zinc Finger Protein Glis2 and Participates in Neuronal Apoptosis Following Intracerebral Hemorrhage.

Abstract

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 p75NTR, a member of the tumor necrosis factor receptor superfamily, was identified both in vivo and in vitro. These experiments further indicated that p75NTR 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 p75NTR-Glis2 complex as a potential reliable treatment for the secondary damage following ICH.