Transcriptome -Wide m6A Methylome and Potential Drug Targets Prediction Analysis of Rheumatoid Arthritis
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ABSTRACT:
PROVIDER: PRJNA795351 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17481751_1.fastq.gz | Fastqsanger.gz | |||
| SRR17481751_2.fastq.gz | Fastqsanger.gz | |||
| SRR17481752_1.fastq.gz | Fastqsanger.gz | |||
| SRR17481752_2.fastq.gz | Fastqsanger.gz | |||
| SRR17481753_1.fastq.gz | Fastqsanger.gz |
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Project description:This research aims at assessing the m6A methylome in the RA peripheral blood mononuclear cells (PBMCs) and perform potential drug targets prediction analysis. Five RA samples and ten control samples were obtained from China-Japan Friendship Hospital. The various expression of m6A methylation and genes in RA and control group were compared with methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq). Bioinformatics explorations were also made to explore the enriched biological roles and paths of the differentially expressed m6A methylation and genes. Potential drug targets prediction and validation were also constructed to provide potential therapeutic targets for RA. In total, 583 dysregulated m6A peaks, of which 295 were greatly upregulated and 288 were greatly downregulated, were identified. Similarly, 1570 differentially genes were acquired by RNA-seq, including 539 upregulated and 1031 downregulated. According to deeper joint exploration, the m6A methylation and mRNA expression degrees of 35 genes varied greatly, of which including 13 hyper-methylated as well as upregulated genes (hyper-up), 12 hyper-methylated and downregulated genes (hyper-down), 5 hypo-methylated as well as upregulated genes (hypo-up), and 5 hypo-methylated and downregulated genes (hypo-down) GO and KEGG explorations showed the enrichment of these distinct genes in “protein transport” “protein binding” and “lysosome”. In addition, the mRNA levels of TUBB2A, IGF2BP3, DYNC1I1 and FOSL1 were increased and consistent with the trend of our sequencing results. While after the treatment of TP and MTX, their mRNA levels were decreased. This research set up the transcriptional map of m6A in RA PBMCs and displayed the hidden association between RNA methylation alternation and associated genes in RA. The outcomes highlight the importance of m6A modification as a gene regulatory system in RA. Furthermore, TUBB2A, IGF2BP3, DYNC1I1 and FOSL1 might be potential therapeutic targets of TP and MTX during RA treatment.
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Project description:Objectives: Epigenetics can influence disease susceptibility and severity. While DNA methylation of individual genes has been explored in autoimmunity, no unbiased systematic analyses have been reported. Therefore, a genome-wide evaluation of DNA methylation loci in fibroblast-like synoviocytes (FLS) isolated from the site of disease in rheumatoid arthritis (RA) was performed. Methods: Genomic DNA was isolated from six RA and five osteoarthritis (OA) FLS lines and evaluated using the Illumina HumanMethylation450 chip. Cluster analysis of data was performed and corrected using Benjamini–Hochberg adjustment for multiple comparisons. Methylation was confirmed by pyrosequencing and gene expression was determined by qPCR. Pathway analysis was performed using the Kyoto Encyclopedia of Genes and Genomes. Results: RA and control FLS segregated based on DNA methylation, with 1859 differentially methylated loci. Hypomethylated loci were identified in key genes relevant to RA, such as CHI3L1, CASP1, STAT3, MAP3K5, MEFV and WISP3. Hypermethylation was also observed, including TGFBR2 and FOXO1. Hypomethylation of individual genes was associated with increased gene expression. Grouped analysis identified 207 hypermethylated or hypomethylated genes with multiple differentially methylated loci, including COL1A1, MEFV and TNF. Hypomethylation was increased in multiple pathways related to cell migration, including focal adhesion, cell adhesion, transendothelial migration and extracellular matrix interactions. Confirmatory studies with OA and normal FLS also demonstrated segregation of RA from control FLS based on methylation pattern. Conclusions: Differentially methylated genes could alter FLS gene expression and contribute to the pathogenesis of RA. DNA methylation of critical genes suggests that RA FLS are imprinted and implicate epigenetic contributions to inflammatory arthritis. Fibroblast-like synoviocyte cell-lines from osteoarthritis (OA) and rheumatoid arthritis (RA) patients.
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Project description:Genome-wide DNA methylation level was studied to determine whether Rheumatoid arthritis patients (cases) has methylation differences comparing to normal controls in PBLs. We used Illumina HumanMethylation450 BeadChip array to determine the genome-wide DNA methylation difference in PBLs from Rheumatoid arthritis patients (cases) and normal controls Bisulphite converted DNA from the Rheumatoid arthritis patients (cases) and normal controls were hybridized to the Illumina Illumina HumanMethylation450 BeadChip arrays
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Project description:With the deepening of epigenetic research, more and more studies have shown that N6- methyladenosine (m6A) is closely related to the occurrence and development of rheumatoid arthritis (RA), but the specific mechanism still needs to be further elucidated. In the study, we collected synovial tissues from normal controls and patients with OA or RA. The levels of m6A and inflammation were analyzed by immunofluorescence and western blot. The role of IGF2BP3 in cell proliferation and inflammatory activation was explored using transfection and RNA immunoprecipitation assays. IGF2BP3-/- mice were established, which were used to construct a mouse model of arthritis by transferring serum from adult arthritis K/BxN mice. Histological analysis and micro-CT were performed to determine joint damage. m6A level was markedly increased in RA patients and mouse models, and the expression of IGF2BP3 was upregulated in RA and related to inflammatory markers. IGF2BP3 played an important part in RA-fibroblast-like synoviocytes (FLS) by promoting cell proliferation, migration, invasion, inflammatory cytokine release, and inhibiting autophagy. In addition, IGF2BP3 inhibited autophagy to reduce the production of ROS, thereby decreasing inflammatory activation in macrophages. More importantly, RASGRF1-mediated mTORC1 activation played a crucial role in the ability of IGF2BP3 to promote cell proliferation and inflammatory activation. Based on the arthritis model of IGF2BP3-/- mice, IGF2BP3 knockdown Inhibited RA-FLS proliferation and inflammatory infiltration, and further improved RA joint injury. Our study revealed the important role of IGF2BP3 in RA progression. The targeted inhibition of IGF2BP3 reduced cell proliferation and inflammatory activation and limited RA development in a mouse model of arthritis, providing a potential strategy for RA therapy.
2025-05-28 | GSE273246 | GEO
Project description:With the deepening of epigenetic research, more and more studies have shown that N6- methyladenosine (m6A) is closely related to the occurrence and development of rheumatoid arthritis (RA), but the specific mechanism still needs to be further elucidated. In the study, we collected synovial tissues from normal controls and patients with OA or RA. The levels of m6A and inflammation were analyzed by immunofluorescence and western blot. The role of IGF2BP3 in cell proliferation and inflammatory activation was explored using transfection and RNA immunoprecipitation assays. IGF2BP3-/- mice were established, which were used to construct a mouse model of arthritis by transferring serum from adult arthritis K/BxN mice. Histological analysis and micro-CT were performed to determine joint damage. m6A level was markedly increased in RA patients and mouse models, and the expression of IGF2BP3 was upregulated in RA and related to inflammatory markers. IGF2BP3 played an important part in RA-fibroblast-like synoviocytes (FLS) by promoting cell proliferation, migration, invasion, inflammatory cytokine release, and inhibiting autophagy. In addition, IGF2BP3 inhibited autophagy to reduce the production of ROS, thereby decreasing inflammatory activation in macrophages. More importantly, RASGRF1-mediated mTORC1 activation played a crucial role in the ability of IGF2BP3 to promote cell proliferation and inflammatory activation. Based on the arthritis model of IGF2BP3-/- mice, IGF2BP3 knockdown Inhibited RA-FLS proliferation and inflammatory infiltration, and further improved RA joint injury. Our study revealed the important role of IGF2BP3 in RA progression. The targeted inhibition of IGF2BP3 reduced cell proliferation and inflammatory activation and limited RA development in a mouse model of arthritis, providing a potential strategy for RA therapy.
2025-05-28 | GSE273245 | GEO