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).
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 have reported that miR-146a-deficient mice developed more severe experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS).
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>).
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.
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.
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.