| Literature DB >> 29339325 |
Min Yan1, Ziyang Liu2, Erkang Fei2, Wenbing Chen2, Xinsheng Lai2, Bin Luo2, Peng Chen2, Hongyang Jing2, Jin-Xiu Pan3, Michael H Rivner4, Wen-Cheng Xiong5, Lin Mei6.
Abstract
Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction (NMJ). Most cases of MG are caused by autoantibodies against the acetylcholine receptor (AChR), muscle-specific kinase (MuSK) and low-density lipoprotein receptor-related protein 4 (LRP4). Recent studies have identified anti-agrin antibodies in MG patients lacking these three antibodies (i.e., triple negative MG). Agrin is a basal lamina protein that has two isoforms. Neural agrin (N-agrin) binds to LRP4 to activate MuSK to induce AChR clusters and is thus critical for NMJ formation. We demonstrate that mice immunized with N-agrin showed MG-associated symptoms including muscle weakness, fragmented and distorted NMJs. These effects were not observed in mice injected with muscle agrin (M-agrin), an isoform that is inactive in inducing AChR clusters. Treatment with anti-N-agrin, but not anti-M-agrin, antibodies reduced agrin-induced AChR clusters in muscle cells. Together, these observations suggest that agrin antibodies may be play a role in MG pathogenesis.Entities:
Keywords: agrin; antibodies; myasthenia gravis; neuromuscular junction
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Year: 2018 PMID: 29339325 PMCID: PMC5942223 DOI: 10.1016/j.neuroscience.2018.01.015
Source DB: PubMed Journal: Neuroscience ISSN: 0306-4522 Impact factor: 3.590