Journal
MUSCLE & NERVE
Volume 57, Issue 5, Pages 814-820Publisher
WILEY
DOI: 10.1002/mus.26025
Keywords
acetylcholine receptor; agrin; myasthenia gravis; neuromuscular junctions
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Funding
- National Basic Research Program of China [2013CB966900]
- National Key-Project of Clinical Neurology, National Science Foundation of China [81230028, 81301044, 81471535]
- Tianjin Education Commission Foundation [14JCYBJC42000]
- US National Institutes of Health [R01NS092713]
- American Heart Association [16SDG27250236]
- National Multiple Sclerosis Society Research [RG-1507-05318]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS092713] Funding Source: NIH RePORTER
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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 Nerve57: 814-820, 2018
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