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Targeting MyD88 Downregulates Inflammatory Mediators and Pathogenic Processes in PBMC From DMARDs-Naïve Rheumatoid Arthritis Patients

ABSTRACT: Targeting MyD88 Downregulates Inflammatory Mediators and Pathogenic Processes in PBMC From DMARDs-Naïve Rheumatoid Arthritis Patients

PROVIDER: PRJNA781616 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16975900_1.fastq.gz	Fastqsanger.gz
	SRR16975900_2.fastq.gz	Fastqsanger.gz
	SRR16975901_1.fastq.gz	Fastqsanger.gz
	SRR16975901_2.fastq.gz	Fastqsanger.gz
	SRR16975883_1.fastq.gz	Fastqsanger.gz

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Targeting MyD88 Downregulates Inflammatory Mediators and Pathogenic Processes in PBMC From DMARDs-Naïve Rheumatoid Arthritis Patients

Project description:Purpose: We analyzed RNA-seq from peripheral blood mononuclear cells (PBMC) in DMARDs-naïve RA patients and healthy subjects. Our goal was to evaluate the transcriptional profiles of ST2825-treated PBMC to identify its therapeutic potential. Methods: We analyzed bulk RNA-seq from peripheral blood mononuclear cells (PBMC) in DMARDs-naïve RA patients after stimulation with LPS and IL-1β, PBMC were treated with the MyD88 chemical inhibitor, ST2825. Collection of RNA was performed after 24 h of treatment and samples were sequenced to determine transcriptional changes and regulated processes in treated PBMC. Results: paired-end reads were mapped to the hg19 human genome assembly. RNA levels were normalized using DESeq. We identified 796 differentially expressed (DE) genes by 2-fold change (p<0.05) between RA patients and healthy subjects. Our analysis revealed 631 DE genes between DMARDs-naïve RA patients before and after ST2825 treatment. We identified 471 DE genes between LPS-stimulated RA PBMC and LPS-stimulated RA PBMC treated with ST2825. Conclusion: Our study provides comprehensive evidence supporting the potential application of the MyD88 inhibitor, ST2825, as a modulator of gene expression signtaures involved in pathogenic processes in PBMC from DMARDs-naïve RA patients. Our indepth analysis of RNA-seq data will serve as a valuable resource containing the inflammatory gene expression signatures by MyD88.

2021-11-30 | GSE189136 | GEO

Targeting MyD88 Downregulates Inflammatory Mediators and Pathogenic Processes in PBMC From DMARDs-Naive Rheumatoid Arthritis Patients.

Project description:MyD88-dependent intracellular signalling cascades and subsequently NF-kappaB-mediated transcription lead to the dynamic inflammatory processes underlying the pathogenesis of rheumatoid arthritis (RA) and related autoimmune diseases. This study aimed to identify the effect of the MyD88 dimerization inhibitor, ST2825, as a modulator of pathogenic gene expression signatures and systemic inflammation in disease-modifying antirheumatic drugs (DMARDs)-naïve RA patients. We analyzed bulk RNA-seq from peripheral blood mononuclear cells (PBMC) in DMARDs-naïve RA patients after stimulation with LPS and IL-1β. The transcriptional profiles of ST2825-treated PBMC were analyzed to identify its therapeutic potential. Ingenuity Pathway Analysis was implemented to identify downregulated pathogenic processes. Our analysis revealed 631 differentially expressed genes between DMARDs-naïve RA patients before and after ST2825 treatment. ST2825-treated RA PBMC exhibited a gene expression signature similar to that of healthy controls PBMC by downregulating the expression of proinflammatory cytokines, chemokines and matrix metalloproteases. In addition, B cell receptor, IL-17 and IL-15 signalling were critically downregulated pathways by ST2825. Furthermore, we identified eight genes (MMP9, CXCL9, MZB1, FUT7, TGM2, IGLV1-51, LINC01010, and CDK1) involved in pathogenic processes that ST2825 can potentially inhibit in distinct cell types within the RA synovium. Overall, our findings indicate that targeting MyD88 effectively downregulates systemic inflammatory mediators and modulates the pathogenic processes in PBMC from DMARDs-naïve RA patients. ST2825 could also potentially inhibit upregulated genes in the RA synovium, preventing synovitis and joint degeneration.

| S-EPMC8735861 | biostudies-literature

RNA-seq of mouse pancreatic pericytes from MyD88-deficient and control mice

Project description:To define pericytic MyD88-dependent expression of cytokines and other immune mediators, pancreatic pericytes were isolated based on their YFP-labeling from Nkx3.2-Cre;EYFP and Nkx3.2-Cre;EYFP;MyD88 flox/flox transgenic mice.

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Juvenile Rheumatoid Arthritis Profiles In PBMC and SFMC

Project description:Biotinylated cRNA was synthesized from total RNA (Enzo; Farmingdale, NY) and processed according to the Affymetrix GeneChip Expression Analysis Technical Manual (Affymetrix; Santa Clara, CA). 57 samples: 5 pauciarticular PBMC, 15 polyarticular PBMC, 11 control PMBC, 6 JSpA PBMC, 5 pauciarticular SFMC, 10 polyarticular PBMC, 5 JSpA SFMC classified by course. Keywords = juvenile rheumatoid arthritis (JRA) Keywords = peripheral blood mononuclear cells (PBMC) Keywords = synovial fluid mononuclear cells (SFMC) Keywords: other

2004-08-11 | GSE1402 | GEO

MYD88 dimerization controls the proliferative, invasive, and pro-inflammatory responses of synovial fibroblasts from rheumatoid arthritis patients

Project description:Purpose: We analyzed RNA-seq from rheumatoid arthritis synovial fibroblats and osteoarthritis syniovial fibroblast patients. Our goal was to evaluate the gene expression signatures after treatment with the MyD88 dimerization onhibitor ST2825 and identify its therapeutic potential. Methods: We analyzed bulk RNA-seq from RA synovial fibroblasts in diferent conditions: Untreated, ST2825-treated, LPS-treated, LPS+ST2825-treated. Aditionally, we analyzed bulk RNA-seq from OA synovial fibroblatss as a control. Collection of RNA was performed after 24 h of treatment and samples were sequenced to determine transcriptional changes and regulated processes. Results: paired-end reads were mapped to the homo sapiens GRCh37 genome assembly. RNA levels were normalized by RPKM and student's t-test. Conclusion: The aggressiveness of the RA SFs, in terms of their proliferation, invasiveness, and increased expression of pain and inflammation mediators was decreased by ST2825. Our data strongly suggest that targeting MyD88 dimerization could mitigate joint inflammation in RA SFs.

2023-09-27 | GSE217012 | GEO

Single cell RNA-seq for PBMC from rheumatoid arthritis patient

Project description:The transcriptome of PBMC from rheumatoid arthritis patient hasn't been compenhensively profiled, and heterogeneous characteristics of blood monocytes in RA patients are much unknown. We performed the single cell transcriptomic analysis of PBMC from rheumatoid arthritis (RA) patient, and monocyte populations were extracted during the analysis. CD127 expression associated expression pattern of inflammatory genes was identified in RA patient's blood monocytes.

2020-11-10 | GSE159117 | GEO

Ad-MyD88 infected MEFs: Control vs. Ad-MyD88 infected

Project description:Transcriptional profiling of Murine Embryonic Fibroblasts (MEFs) infected with Ad-MyD88 vs. Ad-GFP or mock infected. Three-condition experiment, Ad-MyD88 vs. Ad-GFP vs. Mock infected cells. Biological replicates: 3 Ad-MyD88, 3 Ad-GFP, 3 mock, independently grown and harvested. One replicate per array.

2010-01-28 | E-GEOD-18957 | biostudies-arrayexpress

Ad-MyD88 infected bmDCs: Control vs. Ad-MyD88 infected

Project description:Transcriptional profiling of Bone-Marrow derived mouse Dendritic Cells (bmDCs) infected with Ad-MyD88 vs. Ad-GFP or mock infected Three-condition experiment, Ad-MyD88 vs. Ad-GFP vs. Mock infected cells. Biological replicates: 3 Ad-MyD88, 3 Ad-GFP, 3 mock, independently grown and harvested. One replicate per array.

2010-10-08 | E-GEOD-19006 | biostudies-arrayexpress

Expression data from splenocytes - Wild type Myd88 or mutated MYD88-L252P mice

Project description:The MYD88 L265P mutation, activator of NF-kappa B (NF-kB), is found in 80% to 90% of WM. So far, there is no existing animal model for WM to evaluate the role of MYD88 activation, and the only published mouse model harboring the mouse ortholog MYD88 L252P mutation develops aggressive B-cell lymphomas in aged mice. The MYD88 L252P coding sequence was attached to YFP cDNA with an IRES sequence. This construct was flanked with loxP sites and inserted in the Rosa26 locus. The expression of MYD88 L252P protein is induced only in B cells after crossing with CD19_Cre mice.

2021-05-25 | GSE138273 | GEO

MyD88/IL-1R axis sustains immunosuppressive function of TAMs by regulating PD-1 expression in melanoma

Project description:Macrophages are critical mediators of tissue homeostasis, cell proliferation, angiogenesis and tumor metastasis. The presence of TAMs is generally associated with tumor-promoting immunosuppressive function in solid tumors. These macrophages are widely acknowledged as one of the central suppressive populations within tumors, blocking effective T-cell responses. In the present study, we examined the transcriptional landscape of adaptor molecules downstream of TLRs in human cancers and found that higher expression of MYD88 is very well correlated with the tumor progression. In addition, we also found that mouse MyD88 but not TRIF, is essential for tumor progression and angiogenesis in melanoma. Interestingly, MyD88 is critical to maintain the immunosuppressive phenotype of TAMs in the tumors. Moreover, we found that interleukin-1 receptor (IL-1R)-Myd88 axis regulates programmed cell death (PD)-1 expression on TAMs by promoting the recruitment of phospho-NF-κB p65 to the CR-C region of the Pdcd1 promoter. Using myeloid-cell specific MyD88 mutant mice, we also showed that MyD88 expression in myeloid cells alone is sufficient to drive the melanoma progression. Thus, IL-1R/MyD88 axis maintains the immunosuppressive function of tumor-tissue macrophages to promote tumor growth by regulating PD-1/PD-L1 expression

2021-03-26 | GSE137046 | GEO

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