Muscle weakness in myositis: microRNAs mediate dystrophin reduction in MHC class I transgenic mouse model and human muscle biopsies

AbstractObjectiveMuscle inflammation is a feature in myositis and Duchenne Muscular Dystrophy (DMD). Autoimmune mechanisms are thought to contribute to myositis muscle weakness. However, the lack of correlation between inflammatory infiltrates and muscle weakness indicates a role for non ‐immune pathological mechanisms. We previously identified two microRNA sets elevated in DMD muscle. One is an “inflammatory” set that is dampened with glucocorticoids; the other is a “dystrophin‐targeting” set that inhibits dystrophin translation. Here we test the hypothesis that these m iRNAs are similarly dysregulated in myositis muscle and contribute to muscle weakness and disease severity.MethodsWe utilized the MHC class I transgenic myositis mouse model and validated findings in 6 myositis patient muscle biopsies. Mice were classified as mild or severe based on transgene expression, weight, histological severity, and muscle strength/weakness.ResultsSevere myositis mice show mononuclear cell infiltration along with elevated expression of Type 1 IFN and NF ‐B‐regulated genes including Tlr7 (3.8‐fold, p
Source: Arthritis and Rheumatology - Category: Rheumatology Authors: Tags: FULL LENGTH Source Type: research

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ObjectiveMuscle inflammation is a feature in myositis and Duchenne muscular dystrophy (DMD ). Autoimmune mechanisms are thought to contribute to muscle weakness in patients with myositis. However, a lack of correlation between the extent of inflammatory cell infiltration and muscle weakness indicates that nonimmune pathologic mechanisms may play a role. The present study focused on 2 microRNA (miRNA ) sets previously identified as being elevated in the muscle of patients with DMD —an “inflammatory” miRNA set that is dampened with glucocorticoids, and a “dystrophin‐targeting” miRNA set that i...
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