CXCL13 promotes TNF-α synthesis in rheumatoid arthritis through activating ERK/p38 pathway and inhibiting miR-330-3p generation
Copyright © 2024 Elsevier Inc. All rights reserved..
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:221 |
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| Enthalten in: |
Biochemical pharmacology - 221(2024) vom: 31. März, Seite 116037 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Achudhan, David [VerfasserIn] |
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| Links: |
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| Themen: |
CXCL13 |
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| Anmerkungen: |
Date Completed 04.03.2024 Date Revised 04.03.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.bcp.2024.116037 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM367913267 |
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| 520 | |a Copyright © 2024 Elsevier Inc. All rights reserved. | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a CXCL13 | |
| 650 | 4 | |a CXCR5 | |
| 650 | 4 | |a Rheumatoid arthritis | |
| 650 | 4 | |a Synovial fibroblasts | |
| 650 | 4 | |a TNF-α | |
| 650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
| 650 | 7 | |a MicroRNAs |2 NLM | |
| 700 | 1 | |a Lai, Yu-Liang |e verfasserin |4 aut | |
| 700 | 1 | |a Lin, Yen-You |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Yuan-Li |e verfasserin |4 aut | |
| 700 | 1 | |a Tsai, Chun-Hao |e verfasserin |4 aut | |
| 700 | 1 | |a Ho, Trung-Loc |e verfasserin |4 aut | |
| 700 | 1 | |a Ko, Chih-Yuan |e verfasserin |4 aut | |
| 700 | 1 | |a Fong, Yi-Chin |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Chien-Chung |e verfasserin |4 aut | |
| 700 | 1 | |a Tang, Chih-Hsin |e verfasserin |4 aut | |
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