Expression data from myositis muscles
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Wei Zhu
PROVIDER: E-GEOD-39454 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Immune cell infiltration in myositis were by examining microarray expression profiles in muscle biopsies from 31 myositis patients and 5 normal controls.
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Project description:We investigated the gene and exon espression profiling in muscle biopsies of patients affected by inclusion body myosistis, polymyositis and in normal muscle controls
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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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Project description:MHC-I overexpression in muscle biopsies is a hallmark of inflammatory myopathies.However the mechanisms of MHC-I overexpression in each disease is not well understood. Microarray analysis from MHC-I-microdissected myofibers showed a differential expression signature in each inflammatory myopathy. Innate immunity and IFN-I pathways are upregulated vs healthy controls, specifically in dermatomyositis (DM). RNA from MHC-I-positive myofibers were obtained from muscle biopsies of 5 patients with dermatomyositis, 5 with polymyositis, 4 with inclusion body myositis and normal looking fibers from healthy controls.
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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.
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Project description:Idiopathic inflammatory myopathies (IIMs) are severe autoimmune diseases whose pathogenetic mechanisms are still poorly understood. Invalidation of the inducible T cell co-stimulator (Icos) gene on the diabetes-prone NOD mouse background leads to spontaneous autoimmune myositis, providing a tool for studying the pathophysiological mechanisms involved in muscle inflammation. Myositis in Icos-/- NOD mice is characterized by progressive muscle weakness with immune cell infiltration and expression of IFN-associated genes, thus resembling human myositis. Proteomic and spatial transcriptomic analysis of Icos-/- NOD mice muscle brought to light a profound metabolic dysregulation in myofibers. Electron microscopy analysis, mitochondrial respiration assessment and histoenzymology stainings revealed dramatic structural abnormalities and severe dysfunction of muscle mitochondria in diseased Icos-/- NOD mice. Consequently, muscle from these mice exhibited elevated reactive oxygen species (ROS) production and an oxidative stress-transcriptomic signature. Blocking IFN in Icos-/- NOD mice diminished immune cell infiltration and ROS production. Transcriptomic analysis of muscle biopsies from IIMs patients revealed a negative correlation between IFN and mitochondrial gene expression levels, and treatment of human myoblasts with IFN reduced the expression of mitochondrial respiratory chain genes, suggesting a link between IFN production and mitochondrial dysfunction. Sustaining a relevant pathogenic role for oxidative stress in the disease, preventive and therapeutic ROS-buffer treatments also significantly alleviated myositis while preserving mitochondrial ultrastructure and restoring muscle mitochondrial respiration in mice. Notably, preventive ROS-buffer treatment also reduced muscle inflammation. Together, our results suggest that ROS, mitochondrial dysfunction and inflammation are interconnected in a self-maintenance loop, opening perspectives for ROS targeting drugs and/or mitochondria therapy in myositis.
2024-05-31 | PXD048004 | Pride
Project description:Idiopathic inflammatory myopathies (polymyositis and dermatomyositis) are heterogeneous group of muscle disorders of unknown etiology.The pathogenic pathways responsible for muscle fiber damage and dysfunction in myositis are not currently well defined. Identification of such pathways may help to design novel therapeutic interventions and also help to develop diagnostic tests. Keywords: Development or differentiation design
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Project description:Idiopathic inflammatory myopathies (polymyositis and dermatomyositis) are heterogeneous group of muscle disorders of unknown etiology.The pathogenic pathways responsible for muscle fiber damage and dysfunction in myositis are not currently well defined. Identification of such pathways may help to design novel therapeutic interventions and also help to develop diagnostic tests. Experiment Overall Design: Muscle biopsies from a separate group of 5 adult untreated female DM patients were profiled and compared to muscle tissue of normal human healthy volunteers to define molecular pathways in muscle of myositis patients. Confirm and map key pathway members to specific cell types in the muscle tissue of patients and controls using RT-PCR, Western blotting and Immunolocalization.
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Project description:Complement proteins are deposited in the muscles of patients with myositis. However, the local expression and regulation of complement genes within myositis muscle have not been well characterized. In this study, bulk RNA sequencing (RNAseq) analyses of muscle biopsy specimens revealed that complement genes are locally overexpressed and correlate with markers of myositis disease activity, including the expression of interferon-gamma (IFN )-induced genes. Single cell and single nuclei RNAseq analyses showed that most local expression of complement genes occurs in macrophages, fibroblasts, and satellite cells, with each cell type expressing different sets of complement genes. Biopsies from immune-mediated necrotizing myopathy patients, who have the lowest levels of IFN -induced genes, also had the lowest complement gene expression levels. Furthermore, data from cultured human cells showed that IFN upregulates complement expression in macrophages, fibroblasts, and muscle cells. Taken together, our results suggest that in myositis muscle, IFN coordinates the local overexpression of complement genes that occurs in several cell types.
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