The role of beta-catenin signaling pathway on proliferation of rats neural stem cells after hyperbaric oxygen therapy in vitro.

摘要

beta-catenin, a protein that functions in both cell adhesion and Wnt signaling, plays a key role in mammalian neural development. To investigate the role of beta-catenin in hyperbaric oxygen therapy (HBO)-induced neurogenesis after hypoxic ischemic brain damage (HIBD), we transfected beta-catenin siRNA and negative control siRNA into neural stem cells (NSCs) after HIBD. We found that HBO promoted NSCs differentiate into neurons or oligodendrocytes, and inhibited NSCs differentiate into astrocytes; HIBD brain tissue extract conditioned cultures promoted NSCs differentiate into neurons; beta-Catenin siRNA decreased the NSE-positive neurons and increased GFAP-positive astrocytes in the NSCs in vitro. Furthermore, the expression of Ngn1 protein and mRNA in NSCs was increased when HBO promoted NSCs differentiate into neurons after HIBD, and the expression of BMP-4 protein and mRNA was decreased when HBO depressed NSCs differentiate into astrocytes after HIBD. These results showed that beta-catenin-mediated transcriptional activation functions in the decision of NSCs to proliferate neurogenesis during HBO-induced after HIBD, and suggested that HBO therapy promotes the proliferation of neural stem cells in vitro, an effect that may be correlated with beta-catenin protein and HBO therapy could promote neurogenesis by beta-catenin-induced activated Ngn1 gene and repress astrocytogenesis by beta-catenin-induced down-regulated BMP-4 gene.