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CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis

ABSTRACT: CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis

PROVIDER: PRJNA1109863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30681362_1.fastq.gz	Fastqsanger.gz
	SRR30681362_2.fastq.gz	Fastqsanger.gz
	SRR30681363_1.fastq.gz	Fastqsanger.gz
	SRR30681363_2.fastq.gz	Fastqsanger.gz
	SRR30681364_1.fastq.gz	Fastqsanger.gz

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CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis

Project description:Macrophage polarization and synovitis play significant roles in rheumatoid arthritis (RA). Chemokines are involved almost throughout the entire pathology of synovitis. However, the interaction between chemokines and macrophage polarization in RA has been seldom reported. This study found that chemokine C-C motif ligand 7 (CCL7) secreted by polarized M1 macrophages enhances M1 polarization, creating a positive feedback loop and revealing the role of CCL7 in the progression of rheumatoid arthritis. In this research, RNA sequencing indicated that M1 polarized macrophages secrete a large amount of CCL7, which further enhances M1 polarization. Through immunohistochemistry and enzyme-linked immunosorbent assay, it was found that the expression of CCL7 in the synovial tissue and serum of RA patients and mice was upregulated. Intra-articular injection of CCL7 recombinant protein exacerbated M1 polarization of macrophages, inflammation, fibrosis in the synovial tissue, and worsened arthritis pain in mice, which was improved after the injection of CCL7 neutralizing antibody. In addition, CCL7 promoted M1 polarization of macrophages and reversed the M2 polarization induced by IL-4, and it also promoted macrophage proliferation and migration. Although it had an inhibitory effect on chondrocyte activity, it did not show a significant impact on chondrocyte metabolism. Mechanistically, CCL7 targets CCR1 to promote M1 polarization of macrophages, a process partly mediated through the activation of the JAK2/STAT1 pathway. When stimulated by CCL7, macrophages secreted a vast amount of pro-inflammatory factors, exacerbating synovitis and cartilage damage, leading to the aggravation of RA disease. Our research established a positive feedback loop between M1 polarization of macrophages and CCL7, indicating that blocking CCL7 could improve the progression of RA, suggesting CCL7 as a potential target for RA treatment.

2025-01-08 | GSE267151 | GEO

CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis II

2025-01-08 | GSE285977 | GEO

CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis II

Project description:CCL7 promotes macrophage polarization and synovitis to exacerbate rheumatoid arthritis II

| PRJNA1207088 | ENA

Disease activity drives transcriptomic heterogeneity in early untreated rheumatoid synovitis

Project description:Disease activity drives transcriptomic heterogeneity in early untreated rheumatoid synovitis

| PRJNA937236 | ENA

Disease activity drives transcriptomic heterogeneity in early untreated rheumatoid synovitis

Project description:The purpose of this study was to investigate the transcriptomic heterogeneity in synovial tissue of early untreated rheumatoid arthritis patients in association with clinical data

2023-05-31 | GSE225731 | GEO

FABP4 secreted by M1-polarized macrophages promotes synovitis and angiogenesis to exacerbate rheumatoid arthritis.

Project description:Increasing evidence shows that adipokines play a vital role in the development of rheumatoid arthritis (RA). Fatty acid-binding protein 4 (FABP4), a novel adipokine that regulates inflammation and angiogenesis, has been extensively studied in a variety of organs and diseases. However, the effect of FABP4 on RA remains unclear. Here, we found that FABP4 expression was upregulated in synovial M1-polarized macrophages in RA. The increase in FABP4 promoted synovitis, angiogenesis, and cartilage degradation to exacerbate RA progression in vivo and in vitro, whereas BMS309403 (a FABP4 inhibitor) and anagliptin (dipeptidyl peptidase 4 inhibitor) inhibited FABP4 expression in serum and synovial M1-polarized macrophages in mice to alleviate RA progression. Further studies showed that constitutive activation of mammalian target of rapamycin complex 1 (mTORC1) by TSC1 deletion specifically in the myeloid lineage regulated FABP4 expression in macrophages to exacerbate RA progression in mice. In contrast, inhibition of mTORC1 by ras homolog enriched in brain (Rheb1) disruption specifically in the myeloid lineage reduced FABP4 expression in macrophages to attenuate RA development in mice. Our findings established an essential role of FABP4 that is secreted by M1-polarized macrophages in synovitis, angiogenesis, and cartilage degradation in RA. BMS309403 and anagliptin inhibited FABP4 expression in synovial M1-polarized macrophages to alleviate RA development. Hence, FABP4 may represent a potential target for RA therapy.

| S-EPMC9213409 | biostudies-literature

Effects of methotrexate and tofacitinib on gene expression of activated rheumatoid arthritis fibroblast-like synoviocytes

Project description:Activated fibroblast-like synoviocytes (FLS) are drivers of synovitis and structural joint damage in rheumatoid arthritis (RA). Despite the use of disease-modifying drugs, only about 50% of RA patients reach remission in real-world settings. We used an unbiased approach to investigate the effects of standard-of-care methotrexate (MTX) and a Janus kinase inhibitor, tofacitinib (TOFA), on gene expression in RA-FLS, in order to identify untargeted disease mediators.

2024-10-04 | GSE266310 | GEO

Ccl7

Project description:Rattus norvegicus Ccl7, C-C motif chemokine ligand 7 [Source:RGD Symbol;Acc:1359152], is differentially expressed in 24 experiment(s);

| ENSRNOG00000000239 | ExpressionAtlas

Ccl7

Project description:Rattus norvegicus Ccl7, C-C motif chemokine ligand 7 [Source:RGD Symbol;Acc:1359152], is expressed in 6 baseline experiment(s);

| ENSRNOG00000000239 | ExpressionAtlas

CCL7

Project description:Macaca mulatta CCL7, C-C motif chemokine ligand 7 [Source:VGNC Symbol;Acc:VGNC:99133], is expressed in 1 baseline experiment(s);

| ENSMMUG00000009782 | ExpressionAtlas

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