Antibodies against Muscle-Specific Kinase Impair Both Presynaptic and Postsynaptic Functions in a Murine Model of Myasthenia Gravis
Antibodies against acetylcholine receptors (AChRs) cause pathogenicity in myasthenia gravis (MG) patients through complement pathway-mediated destruction of postsynaptic membranes at neuromuscular junctions (NMJs). However, antibodies against muscle-specific kinase (MuSK), which constitute a major s...
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| Veröffentlicht in: | The American journal of pathology 2012-02, Vol.180 (2), p.798-810 |
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| creator | Mori, Shuuichi Kubo, Sachiho Akiyoshi, Takuyu Yamada, Shigeru Miyazaki, Tsuyoshi Hotta, Harumi Desaki, Junzo Kishi, Masahiko Konishi, Tetsuro Nishino, Yuri Miyazawa, Atsuo Maruyama, Naoki Shigemoto, Kazuhiro |
| description | Antibodies against acetylcholine receptors (AChRs) cause pathogenicity in myasthenia gravis (MG) patients through complement pathway-mediated destruction of postsynaptic membranes at neuromuscular junctions (NMJs). However, antibodies against muscle-specific kinase (MuSK), which constitute a major subclass of antibodies found in MG patients, do not activate the complement pathway. To investigate the pathophysiology of MuSK-MG and establish an experimental autoimmune MG (EAMG) model, we injected MuSK protein into mice deficient in complement component five (C5). MuSK-injected mice simultaneously developed severe muscle weakness, accompanied by an electromyographic pattern such as is typically observed in MG patients. In addition, we observed morphological and functional defects in the NMJs of EAMG mice, demonstrating that complement activation is not necessary for the onset of MuSK-MG. Furthermore, MuSK-injected mice exhibited acetylcholinesterase (AChE) inhibitor-evoked cholinergic hypersensitivity, as is observed in MuSK-MG patients, and a decrease in both AChE and the AChE-anchoring protein collagen Q at postsynaptic membranes. These findings suggest that MuSK is indispensable for the maintenance of NMJ structure and function, and that disruption of MuSK activity by autoantibodies causes MG. This mouse model of EAMG could be used to develop appropriate medications for the treatment of MuSK-MG in humans. |
| doi_str_mv | 10.1016/j.ajpath.2011.10.031 |
| format | Article |
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However, antibodies against muscle-specific kinase (MuSK), which constitute a major subclass of antibodies found in MG patients, do not activate the complement pathway. To investigate the pathophysiology of MuSK-MG and establish an experimental autoimmune MG (EAMG) model, we injected MuSK protein into mice deficient in complement component five (C5). MuSK-injected mice simultaneously developed severe muscle weakness, accompanied by an electromyographic pattern such as is typically observed in MG patients. In addition, we observed morphological and functional defects in the NMJs of EAMG mice, demonstrating that complement activation is not necessary for the onset of MuSK-MG. Furthermore, MuSK-injected mice exhibited acetylcholinesterase (AChE) inhibitor-evoked cholinergic hypersensitivity, as is observed in MuSK-MG patients, and a decrease in both AChE and the AChE-anchoring protein collagen Q at postsynaptic membranes. These findings suggest that MuSK is indispensable for the maintenance of NMJ structure and function, and that disruption of MuSK activity by autoantibodies causes MG. This mouse model of EAMG could be used to develop appropriate medications for the treatment of MuSK-MG in humans.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>DOI: 10.1016/j.ajpath.2011.10.031</identifier><identifier>PMID: 22142810</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: Elsevier Inc</publisher><subject>Animals ; Autoantibodies - physiology ; Biological and medical sciences ; Cholinesterase Inhibitors - pharmacology ; Complement C5 - deficiency ; Diseases of striated muscles. Neuromuscular diseases ; Immunoglobulin G - physiology ; Investigative techniques, diagnostic techniques (general aspects) ; Medical sciences ; Mice ; Mice, Inbred Strains ; Muscle Strength - physiology ; Muscle Weakness - immunology ; Myasthenia Gravis, Autoimmune, Experimental - immunology ; Myasthenia Gravis, Autoimmune, Experimental - pathology ; Neurology ; Neuromuscular Junction - immunology ; Neuromuscular Junction - pathology ; Neuromuscular Junction - ultrastructure ; Pathology ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Receptor Protein-Tyrosine Kinases - immunology ; Recombinant Proteins ; Signal Transduction ; Synapses - immunology ; Synapses - pathology ; Synapses - physiology ; Synaptic Transmission - physiology ; Weight Loss - physiology</subject><ispartof>The American journal of pathology, 2012-02, Vol.180 (2), p.798-810</ispartof><rights>American Society for Investigative Pathology</rights><rights>2012 American Society for Investigative Pathology</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-f58bd2f66888dab1299c2bcd6ebfc008ddecd94c8a64e96612468b5d56ae7e983</citedby><cites>FETCH-LOGICAL-c558t-f58bd2f66888dab1299c2bcd6ebfc008ddecd94c8a64e96612468b5d56ae7e983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ajpath.2011.10.031$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25726577$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22142810$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mori, Shuuichi</creatorcontrib><creatorcontrib>Kubo, Sachiho</creatorcontrib><creatorcontrib>Akiyoshi, Takuyu</creatorcontrib><creatorcontrib>Yamada, Shigeru</creatorcontrib><creatorcontrib>Miyazaki, Tsuyoshi</creatorcontrib><creatorcontrib>Hotta, Harumi</creatorcontrib><creatorcontrib>Desaki, Junzo</creatorcontrib><creatorcontrib>Kishi, Masahiko</creatorcontrib><creatorcontrib>Konishi, Tetsuro</creatorcontrib><creatorcontrib>Nishino, Yuri</creatorcontrib><creatorcontrib>Miyazawa, Atsuo</creatorcontrib><creatorcontrib>Maruyama, Naoki</creatorcontrib><creatorcontrib>Shigemoto, Kazuhiro</creatorcontrib><title>Antibodies against Muscle-Specific Kinase Impair Both Presynaptic and Postsynaptic Functions in a Murine Model of Myasthenia Gravis</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>Antibodies against acetylcholine receptors (AChRs) cause pathogenicity in myasthenia gravis (MG) patients through complement pathway-mediated destruction of postsynaptic membranes at neuromuscular junctions (NMJs). However, antibodies against muscle-specific kinase (MuSK), which constitute a major subclass of antibodies found in MG patients, do not activate the complement pathway. To investigate the pathophysiology of MuSK-MG and establish an experimental autoimmune MG (EAMG) model, we injected MuSK protein into mice deficient in complement component five (C5). MuSK-injected mice simultaneously developed severe muscle weakness, accompanied by an electromyographic pattern such as is typically observed in MG patients. In addition, we observed morphological and functional defects in the NMJs of EAMG mice, demonstrating that complement activation is not necessary for the onset of MuSK-MG. Furthermore, MuSK-injected mice exhibited acetylcholinesterase (AChE) inhibitor-evoked cholinergic hypersensitivity, as is observed in MuSK-MG patients, and a decrease in both AChE and the AChE-anchoring protein collagen Q at postsynaptic membranes. These findings suggest that MuSK is indispensable for the maintenance of NMJ structure and function, and that disruption of MuSK activity by autoantibodies causes MG. This mouse model of EAMG could be used to develop appropriate medications for the treatment of MuSK-MG in humans.</description><subject>Animals</subject><subject>Autoantibodies - physiology</subject><subject>Biological and medical sciences</subject><subject>Cholinesterase Inhibitors - pharmacology</subject><subject>Complement C5 - deficiency</subject><subject>Diseases of striated muscles. 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Miscellaneous investigative techniques</subject><subject>Receptor Protein-Tyrosine Kinases - immunology</subject><subject>Recombinant Proteins</subject><subject>Signal Transduction</subject><subject>Synapses - immunology</subject><subject>Synapses - pathology</subject><subject>Synapses - physiology</subject><subject>Synaptic Transmission - physiology</subject><subject>Weight Loss - physiology</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksFu1DAQhiMEoqXwBgj5gjhlsb2x41yQSkVLRVdUKpwtx56wXrJ28DiV9syL42WXInHhZHn8zT_Wp6mql4wuGGXy7WZhNpPJ6wWnjJXSgi7Zo-qUCS5qzjr2uDqllPK6axp6Uj1D3JSrXCr6tDrhnDVcMXpa_TwP2ffReUBivhkfMJPVjHaE-m4C6wdvyScfDAK53k7GJ_I-5jW5TYC7YKZcnk1w5DZifihczsFmHwMSH4gpcckHIKvoYCRxIKudwbyG4A25Sube4_PqyWBGhBfH86z6evnhy8XH-ubz1fXF-U1thVC5HoTqHR-kVEo50zPedZb31knoB0upcg6s6xqrjGygk5LxRqpeOCENtNCp5Vn15pA7pfhjBsx669HCOJoAcUbdsVa0SvwmmwNpU0RMMOgp-a1JO82o3tvXG32wr_f299Viv7S9Og6Y-y24h6Y_ugvw-ggYtGYckgnW419OtFyKti3cuwMHRce9h6TReggWnE9gs3bR_-8n_wbY0QdfZn6HHeAmzikU1Zpp5Jrqu_2m7BeFlUjKl3L5C1Ggu5M</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Mori, Shuuichi</creator><creator>Kubo, Sachiho</creator><creator>Akiyoshi, Takuyu</creator><creator>Yamada, Shigeru</creator><creator>Miyazaki, Tsuyoshi</creator><creator>Hotta, Harumi</creator><creator>Desaki, Junzo</creator><creator>Kishi, Masahiko</creator><creator>Konishi, Tetsuro</creator><creator>Nishino, Yuri</creator><creator>Miyazawa, Atsuo</creator><creator>Maruyama, Naoki</creator><creator>Shigemoto, Kazuhiro</creator><general>Elsevier Inc</general><general>American Society for Investigative Pathology</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20120201</creationdate><title>Antibodies against Muscle-Specific Kinase Impair Both Presynaptic and Postsynaptic Functions in a Murine Model of Myasthenia Gravis</title><author>Mori, Shuuichi ; Kubo, Sachiho ; Akiyoshi, Takuyu ; Yamada, Shigeru ; Miyazaki, Tsuyoshi ; Hotta, Harumi ; Desaki, Junzo ; Kishi, Masahiko ; Konishi, Tetsuro ; Nishino, Yuri ; Miyazawa, Atsuo ; Maruyama, Naoki ; Shigemoto, Kazuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-f58bd2f66888dab1299c2bcd6ebfc008ddecd94c8a64e96612468b5d56ae7e983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Autoantibodies - physiology</topic><topic>Biological and medical sciences</topic><topic>Cholinesterase Inhibitors - pharmacology</topic><topic>Complement C5 - deficiency</topic><topic>Diseases of striated muscles. Neuromuscular diseases</topic><topic>Immunoglobulin G - physiology</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Muscle Strength - physiology</topic><topic>Muscle Weakness - immunology</topic><topic>Myasthenia Gravis, Autoimmune, Experimental - immunology</topic><topic>Myasthenia Gravis, Autoimmune, Experimental - pathology</topic><topic>Neurology</topic><topic>Neuromuscular Junction - immunology</topic><topic>Neuromuscular Junction - pathology</topic><topic>Neuromuscular Junction - ultrastructure</topic><topic>Pathology</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. 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However, antibodies against muscle-specific kinase (MuSK), which constitute a major subclass of antibodies found in MG patients, do not activate the complement pathway. To investigate the pathophysiology of MuSK-MG and establish an experimental autoimmune MG (EAMG) model, we injected MuSK protein into mice deficient in complement component five (C5). MuSK-injected mice simultaneously developed severe muscle weakness, accompanied by an electromyographic pattern such as is typically observed in MG patients. In addition, we observed morphological and functional defects in the NMJs of EAMG mice, demonstrating that complement activation is not necessary for the onset of MuSK-MG. Furthermore, MuSK-injected mice exhibited acetylcholinesterase (AChE) inhibitor-evoked cholinergic hypersensitivity, as is observed in MuSK-MG patients, and a decrease in both AChE and the AChE-anchoring protein collagen Q at postsynaptic membranes. These findings suggest that MuSK is indispensable for the maintenance of NMJ structure and function, and that disruption of MuSK activity by autoantibodies causes MG. This mouse model of EAMG could be used to develop appropriate medications for the treatment of MuSK-MG in humans.</abstract><cop>Bethesda, MD</cop><pub>Elsevier Inc</pub><pmid>22142810</pmid><doi>10.1016/j.ajpath.2011.10.031</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Autoantibodies - physiology Biological and medical sciences Cholinesterase Inhibitors - pharmacology Complement C5 - deficiency Diseases of striated muscles. Neuromuscular diseases Immunoglobulin G - physiology Investigative techniques, diagnostic techniques (general aspects) Medical sciences Mice Mice, Inbred Strains Muscle Strength - physiology Muscle Weakness - immunology Myasthenia Gravis, Autoimmune, Experimental - immunology Myasthenia Gravis, Autoimmune, Experimental - pathology Neurology Neuromuscular Junction - immunology Neuromuscular Junction - pathology Neuromuscular Junction - ultrastructure Pathology Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Receptor Protein-Tyrosine Kinases - immunology Recombinant Proteins Signal Transduction Synapses - immunology Synapses - pathology Synapses - physiology Synaptic Transmission - physiology Weight Loss - physiology |
| title | Antibodies against Muscle-Specific Kinase Impair Both Presynaptic and Postsynaptic Functions in a Murine Model of Myasthenia Gravis |
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