Loss of protein-tyrosine phosphatase α (PTPα) increases proliferation and delays maturation of oligodendrocyte progenitor cells.

摘要: Tightly controlled termination of proliferation determines when oligodendrocyte progenitor cells (OPCs) can initiate differentiation and mature into myelin-forming cells. Protein-tyrosine phosphatase α (PTPα) promotes OPC differentiation, but its role in is unknown. Here we report that loss PTPα enhanced vitro survival decreased cell cycle exit growth factor dependence OPCs not neural stem/progenitor PTPα−/− mice have more lineage embryonic forebrain delayed maturation. On the molecular level, PTPα-deficient mouse rat CG4 Fyn increased Ras, Cdc42, Rac1, Rho activities, reduced expression Cdk inhibitor p27Kip1. Moreover, was required to suppress Ras for p27Kip1 accumulation, inhibition restored We propose PTPα-Fyn signaling negatively regulates by down-regulating Rho, leading accumulation exit. Thus, acts limit self-renewal facilitate differentiation.