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MicroRNA and mRNA profiling in the idiopathic inflammatory myopathies

ABSTRACT: MicroRNA and mRNA profiling in the idiopathic inflammatory myopathies

PROVIDER: PRJNA518143 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8514900_1.fastq.gz	Fastqsanger.gz
	SRR8514900_2.fastq.gz	Fastqsanger.gz
	SRR8514910_1.fastq.gz	Fastqsanger.gz
	SRR8514910_2.fastq.gz	Fastqsanger.gz
	SRR8514920_1.fastq.gz	Fastqsanger.gz

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MicroRNA and mRNA profiling in the idiopathic inflammatory myopathies

Project description:Objectives: The idiopathic inflammatory myopathies (IIMs) are heterogeneous autoimmune conditions of skeletal muscle inflammation and weakness. MicroRNAs (miRNAs) are short, non-coding RNA which regulate gene expression of target mRNAs. The aim of this study was to profile miRNA and mRNA in IIM and identify miRNA-mRNA relationships which may be relevant to disease. Materials and methods: mRNA and miRNA in whole blood samples from 7 polymyositis (PM), 7 dermatomyositis (DM), 5 inclusion body myositis (IBM) and 5 non-myositis controls was profiled using next generation RNA sequencing. Gene ontology and pathway analyses were performed using GOseq and Ingenuity Pathway Analysis. Dysregulation of miRNAs and opposite dysregulation of predicted target mRNAs in IIM subgroups was validated using RTqPCR and investigated by transfecting human skeletal muscle cells with miRNA mimic. Results Analysis of differentially expressed genes showed that interferon signalling and anti-viral response pathways were upregulated in PM and DM compared to controls. An anti-Jo1 autoantibody positive subset of PM and DM (n=5) had more significant upregulation and predicted activation of interferon signalling and highlighted T-helper (Th1 and Th2) cell pathways. In miRNA profiling miR-96-5p was significantly upregulated in PM, DM and the anti-Jo1positive subset. RTqPCR replicated miR-96-5p upregulation and predicted mRNA target (ADK, CD28 and SLC4A10) downregulation. Transfection of a human skeletal muscle cell line with miR-96-5p mimic resulted in significant downregulation of ADK. Conclusion: MiRNA and mRNA profiling identified dysregulation of interferon signalling, anti-viral response and T-helper cell pathways, and indicates a possible role for miR-96-5p regulation of ADK in pathogenesis of IIM.

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The characterization of circulating extracellular vesicles and small non-coding RNAs cargo in idiopathic inflammatory myopathies reveals differences across clinically diagnosed myositis subsets

Project description:Objective. To investigate the epigenetic footprint of idiopathic inflammatory myopathies (IIM) through characterization of circulating extracellular vesicles (EVs) and the expression of EV-derived small non-coding RNAs (sncRNAs).

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MicroRNA and mRNA profiling in the idiopathic inflammatory myopathies.

Project description:BackgroundThe idiopathic inflammatory myopathies (IIMs) are heterogeneous autoimmune conditions of skeletal muscle inflammation and weakness. MicroRNAs (miRNAs) are short, non-coding RNA which regulate gene expression of target mRNAs. The aim of this study was to profile miRNA and mRNA in IIM and identify miRNA-mRNA relationships which may be relevant to disease.MethodsmRNA and miRNA in whole blood samples from 7 polymyositis (PM), 7 dermatomyositis (DM), 5 inclusion body myositis and 5 non-myositis controls was profiled using next generation RNA sequencing. Gene ontology and pathway analyses were performed using GOseq and Ingenuity Pathway Analysis. Dysregulation of miRNAs and opposite dysregulation of predicted target mRNAs in IIM subgroups was validated using RTqPCR and investigated by transfecting human skeletal muscle cells with miRNA mimic.ResultsAnalysis of differentially expressed genes showed that interferon signalling, and anti-viral response pathways were upregulated in PM and DM compared to controls. An anti-Jo1 autoantibody positive subset of PM and DM (n = 5) had more significant upregulation and predicted activation of interferon signalling and highlighted T-helper (Th1 and Th2) cell pathways. In miRNA profiling miR-96-5p was significantly upregulated in PM, DM and the anti-Jo1 positive subset. RTqPCR replicated miR-96-5p upregulation and predicted mRNA target (ADK, CD28 and SLC4A10) downregulation. Transfection of a human skeletal muscle cell line with miR-96-5p mimic resulted in significant downregulation of ADK.ConclusionMiRNA and mRNA profiling identified dysregulation of interferon signalling, anti-viral response and T-helper cell pathways, and indicates a possible role for miR-96-5p regulation of ADK in pathogenesis of IIM.

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Studies in the Natural History and Pathogenesis of Childhood-Onset and Adult-Onset Idiopathic Inflammatory Myopathies

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Immunoglobulin G N-glycosylation associates with novel endotypes of idiopathic inflammatory myopathies patients

Project description:Objectives: This study aimed to investigate the association between immunoglobulin G (IgG) N-glycosylation patterns and the clinical endotypes of patients with idiopathic inflammatory myopathies (IIM), potentially informing disease classification and therapeutic target identification. Methods: We recruited 168 IIM patients and 52 healthy controls, and performed IgG N-glycosylation profiling using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and employed GlycoQuant for intact glycopeptide analysis. Clinical data were extracted, and statistical analyses were conducted to correlate glycosylation profiles with clinical manifestations. Unsupervised clustering analysis was applied to identify novel IIM subgroups based on differential IgG N-glycosylation. Results: Our analysis revealed significant disparities in IgG N-glycosylation between IIM patients and controls, with 13 specific glycoforms exhibiting marked alterations. The level of fucosylated glycans was significantly higher in the IIM patients than healthy controls. Three distinct IIM endotypes were identified, each characterized by unique glycosylation signatures and clinical phenotypes. These endotypes were not congruent with conventional diagnostic subgroups and demonstrated associations with various clinical outcomes, including muscle weakness, interstitial lung disease (ILD), and serological profiles.

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Idiopathic inflammatory myopathies.

Project description:The idiopathic inflammatory myopathies (IIM) consist of rare heterogeneous autoimmune disorders that present with marked proximal and symmetric muscle weakness, except for distal and asymmetric weakness in inclusion body myositis. Despite many similarities, the IIM are fairly heterogeneous from the histopathologic and pathogenetic standpoints, and also show some clinical and treatment-response differences. The field has witnessed significant advances in our understanding of the pathophysiology and treatment of these rare disorders. This review focuses on dermatomyositis, polymyositis, and necrotizing myopathy, and examines current and promising therapies.

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