M1 and M2 Functional Imprinting of Primary Microglia: Role of P2X7 Activation and miR-125b.

摘要: Amyotrophic lateral sclerosis (ALS) is a most frequently occurring and severe form of motor neuron disease, causing death within 3–5 years from diagnosis with worldwide incidence about 2 per 100,000 person-years. Mutations in over twenty genes associated familial forms ALS have provided insights into the mechanisms leading to death. Moreover, mutations two RNA binding proteins, TAR DNA protein 43 fused sarcoma, raised intriguing possibility that perturbations metabolism, including small endogenous molecules repress target at posttranscriptional level, is, microRNAs, may contribute disease pathogenesis. At present, by which microglia actively participate both toxic neuroprotective actions constitute an important matter research. Among pathways involved ALS-altered responses, previous works we uncovered hyperactivation P2X7 receptor extracellular ATP overexpression miR-125b, uncontrolled M1 reactions. In order shed further light on complexity these processes, this short review will describe M1/M2 functional imprinting primary role played miR-125b activation.