Rbfox-1 contributes to CaMKIIα expression and intracerebral hemorrhage-induced secondary brain injury via blocking micro-RNA-124:

摘要: RNA-binding protein fox-1 homolog 1 (Rbfox-1), an in neurons, is thought to be associated with many neurological diseases. To date, the mechanism on which Rbfox-1 worsens secondary cell death ICH remains poorly understood. In this study, we aimed explore role of intracerebral hemorrhage (ICH)-induced brain injury (SBI) and identify its underlying mechanisms. We found that expression neurons was significantly increased after ICH, accompanied by increases binding Ca2+/calmodulin-dependent kinase II (CaMKIIα) mRNA level CaMKIIα. addition, when exposed exogenous upregulation or downregulation Rbfox-1, CaMKIIα showed a concomitant trend tissue, further suggested downstream-target Rbfox-1. The both proteins caused intracellular-Ca2+ overload neuronal degeneration, exacerbated damage. Furthermore, promoted via blocking micro-RNA-124 mRNA. Thus, expected promising therapeutic target for SBI ICH.