{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,4]],"date-time":"2023-10-04T06:11:50Z","timestamp":1696399910595},"reference-count":35,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,10,31]],"date-time":"2013-10-31T00:00:00Z","timestamp":1383177600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int J Experimental Path"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The aim of this study is to determine whether primary over\u2010expression of A\u03b2<jats:styled-content style=\"fixed-case\">PP<\/jats:styled-content> in skeletal muscle results in the development of features of inclusion body myositis (<jats:styled-content style=\"fixed-case\">IBM<\/jats:styled-content>) in a new lineage of the <jats:italic><jats:styled-content style=\"fixed-case\">MCK<\/jats:styled-content>\u2010A\u03b2<jats:styled-content style=\"fixed-case\">PP<\/jats:styled-content><\/jats:italic> transgenic mouse. Quantitative histological, immunohistochemical and western blotting studies were performed on muscles from 3 to 18\u00a0month old transgenic and wild\u2010type C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>6\/<jats:styled-content style=\"fixed-case\">SJL<\/jats:styled-content> mice. Electron microscopy was also performed on muscle sections from selected animals. Although western blotting confirmed that there was over\u2010expression of full length A\u03b2<jats:styled-content style=\"fixed-case\">PP<\/jats:styled-content> in transgenic mouse muscles, deposition of amyloid\u2010\u03b2 and fibrillar amyloid could not be demonstrated histochemically or with electron microscopy. Additionally, other changes typical of <jats:styled-content style=\"fixed-case\">IBM<\/jats:styled-content> such as rimmed vacuoles, cytochrome C oxidase\u2010deficient fibres, upregulation of <jats:styled-content style=\"fixed-case\">MHC<\/jats:styled-content> antigens, lymphocytic inflammatory infiltration and T cell fibre invasion were absent. The most prominent finding in both transgenic and wild\u2010type animals was the presence of tubular aggregates which was age\u2010related and largely restricted to male animals. Expression of full length A\u03b2<jats:styled-content style=\"fixed-case\">PP<\/jats:styled-content> in this <jats:italic><jats:styled-content style=\"fixed-case\">MCK<\/jats:styled-content>\u2010A\u03b2<jats:styled-content style=\"fixed-case\">PP<\/jats:styled-content><\/jats:italic> mouse lineage did not reach the levels required for immunodetection or deposition of amyloid\u2010\u03b2 as in the original transgenic strains, and was not associated with the development of pathological features of <jats:styled-content style=\"fixed-case\">IBM<\/jats:styled-content>. These negative results emphasise the potential pitfalls of re\u2010deriving transgenic mouse strains in different laboratories.<\/jats:p>","DOI":"10.1111\/iep.12048","type":"journal-article","created":{"date-parts":[[2013,10,31]],"date-time":"2013-10-31T11:04:04Z","timestamp":1383217444000},"page":"418-425","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Primary over\u2010expression of A\u03b2<scp>PP<\/scp> in muscle does not lead to the development of inclusion body myositis in a new lineage of the <i><scp>MCK<\/scp>\u2010A\u03b2<scp>PP<\/scp><\/i> transgenic mouse"],"prefix":"10.1111","volume":"94","author":[{"given":"Yue\u2010Bei","family":"Luo","sequence":"first","affiliation":[{"name":"Centre for Neuromuscular and Neurological Disorders Australian Neuro\u2010muscular Research Institute University of Western Australia Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Russell D.","family":"Johnsen","sequence":"additional","affiliation":[{"name":"Centre for Neuromuscular and Neurological Disorders Australian Neuro\u2010muscular Research Institute University of Western Australia Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lisa","family":"Griffiths","sequence":"additional","affiliation":[{"name":"Section of Neuropathology Department of Anatomical Pathology Royal Perth Hospital Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Merrilee","family":"Needham","sequence":"additional","affiliation":[{"name":"Centre for Neuromuscular and Neurological Disorders Australian Neuro\u2010muscular Research Institute University of Western Australia Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Victoria A.","family":"Fabian","sequence":"additional","affiliation":[{"name":"Section of Neuropathology Department of Anatomical Pathology Royal Perth Hospital Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sue","family":"Fletcher","sequence":"additional","affiliation":[{"name":"Centre for Neuromuscular and Neurological Disorders Australian Neuro\u2010muscular Research Institute University of Western Australia Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steve D.","family":"Wilton","sequence":"additional","affiliation":[{"name":"Centre for Neuromuscular and Neurological Disorders Australian Neuro\u2010muscular Research Institute University of Western Australia Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frank L.","family":"Mastaglia","sequence":"additional","affiliation":[{"name":"Centre for Neuromuscular and Neurological Disorders Australian Neuro\u2010muscular Research Institute University of Western Australia Perth WA Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2013,10,31]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/00002281-200311000-00009"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.3.1314"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/bit.10517"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2010.05.018"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.molbrainres.2004.08.006"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M112.359588"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1080\/01926230490520232"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1212\/01.wnl.0000192129.65677.87"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1085\/JGP1322OIA1"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2011.03.007"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1096\/fj.03-0978fje"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2008.12.002"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.274.5284.99"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-328X(96)00161-1"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1150-09.2009"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/0169-328X(91)90010-U"},{"key":"e_1_2_7_18_1","first-page":"315","article-title":"Increased amyloid\u2010\u03b2 levels in APPSWE transgenic mice treated chronically with a physiological high\u2010fat high\u2010cholesterol diet","volume":"6","author":"Levin\u2010Allerhand J.A.","year":"2002","journal-title":"J. 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