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

ABSTRACT: 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].

ORGANISM(S): Mus musculus

SUBMITTER: Carsten Sticht

PROVIDER: E-GEOD-33157 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2011-12-09 | GSE33157 | GEO

Gene expression analysis of FSHD muscle with different MRI pattern

Project description:Objective: to focus on the molecular mechanisms involved in the dystrophic process that leads to selective wasting of single muscles or muscle groups in Facioscapulohumeral muscular dystrophy (FSHD). By muscle MRI we observed that T2-short tau inversion recovery (T2-STIR) sequences identify two different patterns in which each muscle can be found before the irreversible dystrophic alteration, marked as T1-weighted sequence hyperintensity. We studied these conditions in order to obtain further information on the disease pathogenesis. Design: histopathology, gene expression profiling and real time PCR were performed on muscle biopsies. Subjects: muscles (n=8) with different MRI pattern (T1-weighted normal/T2-STIR normal and T1-weighted normal/T2-STIR hyperintense) from FSHD patients. Data were also compared with inflammatory myopathies (n=7), dysferlinopathies (n=4) and normal controls (n=7). Results: myopathic and inflammatory changes characterize T2-STIR hyperintense FSHD muscles, at variance with T2-STIR normal muscles. These two states can be easily distinguished from each other by their transcriptional profile. Comparison of T2-STIR hyperintense FSHD muscles with muscles of inflammatory myopathies shows peculiar changes, although many alterations are shared among these conditions. Conclusions: at the single muscle level, different stages of the disease correspond to the two MRI patterns. T2-STIR hyperintense FSHD muscles are more similar to inflammatory myopathies than to T2-STIR normal FSHD muscles or other muscular dystrophies, and share with them upregulation of genes involved in innate and adaptive immunity. Our data suggest that selective inflammation, together with perturbation in biological processes such as neoangiogenesis, lipid metabolism and adipokine production, may play a role in FSHD progression. 26 samples of human muscle muscle tissue were analysed using the Illumina beadchip technology.

2012-09-14 | E-GEOD-26852 | biostudies-arrayexpress

Gene expression analysis of FSHD muscle with different MRI pattern

2012-09-14 | GSE26852 | GEO

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

Project description: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.

2020-09-22 | GSE158283 | GEO

microRNA expression data from a heterozygous Titin-deficient mouse model and wildtype controls

Project description:Mutations in the sarcomeric protein titin are a major cause of human dilated cardiomyopathy. We have developed a knock-in mouse model that imitated a previously identified titin truncation mutation. The heterotygous Ttn-deficient mice develop features of DCM and therefore recapitulate the human phenotype. To investigate the role of microRNAs in titin-based heart failure, we performed a miRNA screen in heterozygous Ttn-deficient mice and their wildtype littermate controls.

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Muscle stem cells give rise to rhabdomyosarcomas in severe model of Duchenne muscular dystrophy

Project description:We identified muscles as cells of origin of rhabdomyosarcoma in dystrophic mice

2019-01-01 | GSE123423 | GEO

fhl2b expression ameliorates muscular dystrophy [5dpf trunk]

Project description:In muscle dystrophies, muscle fibers loose integrity and die, leading to significant suffering and a shorter life. Strikingly, the extraocular muscles (EOMs), controlling eye movements, are spared and function well despite the disease progression. Although EOMs have been shown to have important differences compared to body musculature the mechanisms underlying this inherent resistance to muscle dystrophies remain largely unknown. Here, we demonstrate important differences in gene expression as a response to muscle dystrophies between the EOMs and trunk muscle in zebrafish via transcriptomic profiling. We show that the LIM-protein Fhl2 is upregulated in response to knockout of desmin, plectin and obscurin, intermediate filament proteins causing different muscle dystrophies, and contributes to disease protection of the EOMs. Moreover, we show that ectopic expression of fhl2b can partially rescue the muscle phenotype in the zebrafish Duchenne muscular dystrophy model sapje, significantly improving their survival rate. Therefore, fhl2 is a protective agent and a candidate target gene for therapy of muscle dystrophies.

2024-02-08 | GSE242135 | GEO

fhl2b expression ameliorates muscular dystrophy [20 months EOM and trunk]

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fhl2b expression ameliorates muscular dystrophy [5 months EOM and trunk]

2024-02-08 | GSE242136 | GEO

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.

2022-08-08 | GSE210263 | GEO

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