Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4343911 | Neuroscience Letters | 2013 | 6 Pages |
Abstract
The purpose of this study was to analyze the expression of miR-146a in PBMCs obtained from patients with myasthenia gravis (MG) and healthy controls and to investigate the effect of the inhibition of miR-146a on the activation of AchR specific B cells obtained from mice. The expression of miR-146a levels in PBMCs obtained from patients with MG and healthy controls were determined by qRT-PCR. MiR-146a's complementary fragment, AntagomiR-146a, was synthesized as inhibitor, and the nonfunctional fragment, which has similar construction to AntagomiR-146a, was synthesized as negative control inhibitor. The expression of miR-146a, CD40, CD80 and CD86 on AchR specific B cells were analyzed by qRT-PCR and flow cytometry. Western blotting was used to detect the expression of TLR4, NF-κB and Bcl-2 .The expression of miRNA-146a in PBMCs obtained from patients with MG was significantly upregulated compared to healthy controls (P < 0.01). Transfection with miR-146a inhibitor dramatically decreased expression of miR-146a, CD40, CD80, TLR4 and NF-κB on AchR specific B cells compared to mock transfected cells. We conclude that abnormal expression/regulation of miR-146a may play an important role in the regulation of AchR specific B cells and contribute to the pathogenesis of MG.
Keywords
TLR4TRAF-6miRNA-146aMicroRNA-146aEAMGNF-κBPBMCsAChRNMJRheumatoid arthritisNeuromuscular junctionmiR-146aperipheral blood mononuclear cellsIRAK-1TNF receptor associated factor 6nuclear factor-κBB cellSystemic lupus erythematosusSLEToll like receptor 4experimental autoimmune myasthenia gravisMyasthenia gravisacetylcholine receptor
Related Topics
Life Sciences
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Neuroscience (General)
Authors
Jiayin Lu, Mei Yan, Yuzhong Wang, Junmei Zhang, Huan Yang, Fa-fa Tian, Wenbin Zhou, Ning Zhang, Jing Li,