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- W4313385559 abstract "Abstract Myasthenia gravis is an autoimmune disorder of the neuromuscular junction manifestated as fatigable muscle weakness. The disorder typically caused by pathogenic autoantibodies against the postsynaptic acetylcholine receptor in the endplate of skeletal muscle. Our previous studies have identified carbonic anhydrase III as a specific protein insufficient in skeletal muscle from myasthenia gravis patient. In this study, we determined to investigate the underlying mechanism how carbonic anhydrase III insufficiency contributes to myasthenia gravis. Based on experimental autoimmune myasthenia gravis animal model and myocyte C2C12 cells, we find that inhibition of carbonic anhydrase III promotes acetylcholine receptor, which is through lipid raft-mediated pathway, leading to accelerated degradation of surface acetylcholine receptor. While activation of carbonic anhydrase III negatively regulates acetylcholine receptor degradation, through suppressing the endocytosis of surface acetylcholine receptor, thus contributes to attenuation of myasthenia gravis. Further study demonstrates that carbonic anhydrase III regulates endocytosis of AChR through actin polymerization and Src phosphorylation. Collectively, our study illustrates that carbonic anhydrase III in skeletal muscle cells is critical for acetylcholine receptor homeostasis in neuromuscular junction, while carbonic anhydrase III deficiency induces accelerated degradation of acetylcholine receptor, leading to myasthenia gravis. This novel mechanism highlights the essential role of carbonic anhydrase III in regualtion acetylcholine receptor endocytosis, providing a potential therapeutic approaches for myasthenia gravis." @default.
- W4313385559 created "2023-01-06" @default.
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- W4313385559 date "2016-05-01" @default.
- W4313385559 modified "2023-09-24" @default.
- W4313385559 title "Suppression of acetylcholine receptor endocytosis in neuromuscular junction by carbonic anhydrase III in the pathogenesis of myasthenia gravis." @default.
- W4313385559 doi "https://doi.org/10.4049/jimmunol.196.supp.118.5" @default.
- W4313385559 hasPublicationYear "2016" @default.
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