Induced neural stem cell grafts exert neuroprotection through an interaction between Crry and Akt in a mouse model of closed head injury

Abstract Background Recently, growing evidence has indicated an important role of the complement system, a crucial component immunity, in mediating neuroinflammation and promoting neuronal apoptosis following closed head injury (CHI). We previously reported that transplanted induced neural stem cells (iNSCs) pre-treated with CHI mouse serum could enhance receptor type 1-related protein y (Crry) expression ameliorate complement-mediated damage models. However, mechanism underlying elevated levels Crry remains elusive. Methods models were established using standardized weight-drop device. collected at 12 h post-trauma. RT-QPCR assay, western blot analysis, deposition Akt inhibition flow cytometry, cell transplantation, functional assay utilized to clarify iNSCs receiving treatment. Results observed dramatic increases activation Remarkably, led reduction iNSCs. Intriguingly, treatment iNSC-derived neurons recombinant 2-conjugated (CR2-Crry), which inhibits all pathways, substantially enhanced after In subsequent vitro experiments pre-treatment CR2-Crry, we significant astrocytes post-treatment serum. Additionally, vivo study showed intracerebral-transplanted CR2-Crry markedly protected from complement-dependent brains mice. Conclusion INSCs increased attenuated CHI.