Engineered agrin attenuates the severity of experimental autoimmune myasthenia gravis |
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| Authors: | Zhiguo Li MS Minshu Li PhD Kristofer Wood BS Steffan Hettwer PhD Suraj A. Muley MD Fu‐Dong Shi MD PhD Qiang Liu MD PhD Shafeeq S. Ladha MD |
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| Affiliation: | 1. Department of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona, USA;2. Neurotune AG, Schlieren‐Zurich, Switzerland;3. Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China |
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| Abstract: | ![]()
Introduction: Agrin is essential for the formation and maintenance of neuromuscular junctions (NMJs). NT‐1654 is a C‐terminal fragment of mouse neural agrin. In this study, we determined the effects of NT‐1654 on the severity of experimental autoimmune myasthenia gravis (EAMG). Methods: EAMG was induced in female Lewis rats by immunization with the Torpedo acetylcholine receptor (tAChR) and complete Freund's adjuvant (CFA). NT‐1654 was dissolved in phosphate‐buffered saline (PBS) and injected daily subcutaneously into tAChR immunized rats during the first 10 days after immunization, and then every other day for the following 20 days. Results: We showed that NT‐1654 attenuated clinical severity, effectively promoted the clustering of AChRs at NMJs, and alleviated the impairment of NMJ transmission and the reduction of muscle‐specific kinase (MuSK) in EAMG rats. Discussion: We demonstrated that NT‐1654 attenuated clinical severity, effectively promoted the clustering of AChRs at NMJs, and alleviated the impairment of NMJ transmission and the reduction of muscle‐specific kinase (MuSK) in EAMG rats. Muscle Nerve 57 : 814–820, 2018 |
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| Keywords: | acetylcholine receptor agrin myasthenia gravis neuromuscular junctions |
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