{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:28:44Z","timestamp":1791300524503,"version":"4.1.0"},"reference-count":25,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2009,11,30]],"date-time":"2009-11-30T00:00:00Z","timestamp":1259539200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2009,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Autoantibodies against the chromatin remodeler Mi\u20102 are found in a distinct subset of patients with dermatomyositis (DM). Previous quantitative immunoblotting experiments demonstrated that Mi\u20102 protein levels are up\u2010regulated in DM muscle. This study was undertaken to define the population of cells expressing high levels of Mi\u20102 in DM muscle and to explore the regulation and functional role of Mi\u20102 during muscle regeneration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The expression of Mi\u20102 was analyzed by immunofluorescence microscopy in human muscle biopsy specimens. In an experimental mouse model, cardiotoxin was used to induce muscle injury and repair, and expression of Mi\u20102 during muscle regeneration was studied in this model by immunofluorescence and immunoblotting analyses. In addition, a cell culture system of muscle differentiation was utilized to artificially modulate Mi\u20102 levels during proliferation and differentiation of myoblasts.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In human DM muscle tissue, increased Mi\u20102 expression was found preferentially in the myofibers within fascicles affected by perifascicular atrophy, particularly in the centralized nuclei of small perifascicular muscle fibers expressing markers of regeneration. In injured mouse muscle tissue, Mi\u20102 levels were dramatically and persistently up\u2010regulated during muscle regeneration in vivo. Premature silencing of Mi\u20102 with RNA interference in vitro resulted in accelerated myoblast differentiation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Expression of Mi\u20102 is markedly up\u2010regulated during muscle regeneration in a mouse model of muscle injury and repair. It is also up\u2010regulated in human DM myofibers expressing markers of regeneration. Results of the in vitro studies indicate that this protein may play a role in modulating the kinetics of myoblast differentiation. Our findings thus suggest that high levels of Mi\u20102 expression in muscle biopsy tissue from patients with DM reflect the presence of incompletely differentiated muscle cells.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.24977","type":"journal-article","created":{"date-parts":[[2009,11,30]],"date-time":"2009-11-30T18:13:25Z","timestamp":1259604805000},"page":"3784-3793","source":"Crossref","is-referenced-by-count":79,"title":["Expression of the dermatomyositis autoantigen Mi\u20102 in regenerating muscle"],"prefix":"10.1002","volume":"60","author":[{"given":"Andrew L.","family":"Mammen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Livia A.","family":"Casciola\u2010Rosen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John C.","family":"Hall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa","family":"Christopher\u2010Stine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea M.","family":"Corse","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antony","family":"Rosen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,11,30]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/ncprheum0760"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)14368-1"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.berh.2004.02.009"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1080\/08916930400022681"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/art.1780280711"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0090-1229(76)90145-8"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-199111000-00002"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1136\/ard.2005.040717"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0889-857X(02)00032-7"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20041367"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(00)00343-2"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1242\/dev.001750"},{"key":"e_1_2_6_14_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.10.5459"},{"key":"e_1_2_6_15_2","doi-asserted-by":"publisher","DOI":"10.1038\/270725a0"},{"key":"e_1_2_6_16_2","unstructured":"Washington University Neuromuscular Disease Center. 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