Taken together, these observations indicate probable implication of complement system and miR-146a in course of immune-related diseases and reveal more facts about the pathogenesis of MS.
Genotyping for miRNA-146a (rs2910164) and its target gene IRAK1 (rs3027898) was performed using real-time polymerase chain reaction (RT-PCR) in 80 patients with SLE and 70 patients with MS, as well as 120 healthy control individuals.
Here, we tested this hypothesis using exogenous miR-146a mimics and a mouse model of MS, experimental autoimmune encephalomyelitis (EAE) induced by immunization with myelin proteolipid protein peptide (PLP<sub>139-151</sub>).
We further investigated the role of miR-146a in miR-146a-deficient (KO) mice: this miRNA is differentially expressed in MS lesions and promotes differentiation of oligodendrocyte precursor cells (OPCs) during remyelination, but its role has not been examined during demyelination.
Here, we have reported that miR-146a-deficient mice developed more severe experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS).
The aim of the present study was to analyze the potential association between two functional miR-146a polymorphisms (rs2910164 and rs57095329) and multiple sclerosis (MS) in the Han Chinese population.
A statistically significant increased expression of miR-21, miR-146a and -b was observed in relapsing remitting (RR)MS patients as compared with controls (1.44±0.13 vs 0.79±0.06, P=0.036; 1.50±0.12 vs 0.84±0.08, P=0.039; 1.54±0.15 vs 0.72±0.08, P=0.001 respectively).