Reference - Detail
| RRC ID | 79279 |
|---|---|
| Author | Achudhan D, Lai YL, Lin YY, Huang YL, Tsai CH, Ho TL, Ko CY, Fong YC, Huang CC, Tang CH. |
| Title | CXCL13 promotes TNF-α synthesis in rheumatoid arthritis through activating ERK/p38 pathway and inhibiting miR-330-3p generation. |
| Journal | Biochem Pharmacol |
| Abstract |
Rheumatoid arthritis (RA) is a well-known autoimmune disorder associated with joint pain, joint swelling, cartilage and bone degradation as well as deformity. The chemokine (C-X-C motif) ligand 13 (CXCL13) plays a crucial role in multiple cellular pathogenesis processes, including RA. TNF-α is a vital proinflammatory factor in the progression of RA. However, the role of CXCL13 in TNF-α production in RA has not been fully explored. Our analysis of both database and clinical samples revealed higher levels of CXCL13 and TNF-α in RA samples compared to healthy controls. CXCL13 concentration-dependently induces TNF-α synthesis in RA synovial fibroblasts. CXCL13 enhances TNF-α expression by interacting with the CXCR5 receptor, activating the ERK/p38 pathways, and inhibiting miR-330-3p generation. Importantly, treatment with CXCL13 shRNA counteracted the upregulation of TNF-α production induced by collagen-induced arthritis. Our findings support the notion that CXCL13 is a promising target in the treatment of RA. |
| Volume | 221 |
| Pages | 116037 |
| Published | 2024-3-1 |
| DOI | 10.1016/j.bcp.2024.116037 |
| PII | S0006-2952(24)00020-0 |
| PMID | 38301965 |
| MeSH | Animals Arthritis, Experimental* Arthritis, Rheumatoid* / genetics Autoimmune Diseases* MicroRNAs* / genetics Tumor Necrosis Factor-alpha / pharmacology |
| IF | 4.96 |
| Altmetric score |
オルトメトリクス指標項目
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| The most frequently cited source | X(Twitter) |
| Total number of mentions | 1 |
| Altmetric score changes over past 6months | 0.0 |
| Resource | |
| Human and Animal Cells | MH7A(RCB1512) |