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Comparative transcriptomic study of skeletal muscles response to muscular dystrophy with myositis

ABSTRACT: Muscular dystrophy with myositis (mdm) is a severe degenerative muscle disease arising from a spontaneous mutaton at the N2A-PEVK junction of titin protein. The affected mice show a complex disease phenotype, and more organism-wide spread response compared to other myopathies. The project objectives forcus on undertanding the response pattetern of different skelelal muscles to mdm.

ORGANISM(S): Mus musculus

PROVIDER: GSE158283 | GEO | 2020/09/22

REPOSITORIES: GEO

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Transcriptomic profiles of muscular dystrophy with myositis (mdm) in extensor digitorum longus, psoas, and soleus muscles from mice

Project description:Titinopathies are inherited muscular diseases triggered by genetic mutations in the titin gene. Muscular dystrophy with myositis (mdm) is one such disease caused by a deletion in the N2A-PEVK region of titin, one of the most active binding sites in titin, and mice with this deletion develop progressive muscle degeneration. The range of phenotypic differences observed in mdm mice extends well beyond impacts on titin, making it clear that deletion of this region initiates a cascade of additional transcriptomic changes. Previous research has focused on correlating phenotypic differences with muscle function in mdm mice. These studies have provided understanding of the downstream physiological effects resulting from the deletion but only provide insights on processes that can be physiologically observed and measured. We used differential gene expression (DGE) to compare the transcriptomes of extensor digitorum longus (EDL), psoas and soleus muscles from wild-type and mdm mice to develop a deeper understand of these tissue-specific responses.

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Sarcolipin is a potential biomarker for dystrophy and is involved in inflammatory processes in skeletal muscles

Project description:Myopathies and muscular dystrophies are devastating diseases sharing characteristic symp-toms. Little is known about common aetiopathology and biomarkers are rare. We studied skeletal muscle gene expression in mouse models of myopathies. As dystrophic processes in muscles are characterised by inflammatory processes, we expanded our analy-sis on a rat model of sepsis. We find 25 commonly dysregulated genes. Sarcolipin was upregulated most, exhibiting in-creased protein levels in different muscles as well as in rats treated with an inflammatory agent. Upregulation strongly correlated with disease status. Our findings suggest Sarcolipin as a potential biomarker and imply a new function in inflam-matory response. Comparison of the expression profile of quadriceps in 2 B6C3Fe a/a-Ttnmdm/J mice with Titin-mutation versus the expression profile of 2 mice without the mutation in Titin [Ttn].

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Comparative transcriptomic study of skeletal muscles response to muscular dystrophy with myositis

Project description:Comparative transcriptomic study of skeletal muscles response to muscular dystrophy with myositis

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Transcription profiling of human muscle biopsies from pre-treatment dermatomyostitis patients vs. normal controls to define molecular pathways in muscle of myositis patients.

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Project description:Tibial muscular dystrophy (TMD) is a late onset, autosomal dominant distal myopathy that results from mutations in the two last domains of titin. The cascade of molecular events leading from the causative Titin mutations to the preterm death of muscle cells in TMD is largely unknown. To identify these components, we used gene expression profiling of muscle biopsies from TMD patients and healthy controls. 5 muscle samples from 2 normal control subjects and muscle samples from 7 TMD subjects.

2014-03-11 | E-GEOD-42806 | biostudies-arrayexpress

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Project description:Expression profiling of human myositis muscle samples This study was designed to compare expression signatures among the various types of inflammatory myopathy, dermatomyositis (DM), inclusion body myositis (IBM), necrotizing myopathy (NM), nonspecific myopathy (NS), and polymyositis (PM) compared to normal (NL) muscle.

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