Open Access

Ubiquitin D promotes the progression of rheumatoid arthritis via activation of the p38 MAPK pathway

  • Authors:
    • Hong Chen
    • Liju Tao
    • Juhua Liang
    • Chunfeng Pan
    • Hua Wei
  • View Affiliations

  • Published online on: January 18, 2023     https://doi.org/10.3892/mmr.2023.12940
  • Article Number: 53
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ubiquitin D (UBD), a member of the ubiquitin‑like modifier family, has been reported to be highly expressed in various types of cancer and its overexpression is positively associated with tumor progression. However, the role and mechanism of UBD in rheumatoid arthritis (RA) remain elusive. In the present study, the gene expression profiles of GSE55457 were downloaded from the Gene Expression Omnibus database to assess differentially expressed genes and perform functional enrichment analyses. UBD was overexpressed by lentivirus transfection. The protein level of UBD, p‑p38 and p38 in RA‑fibroblast‑like synoviocytes (FLSs) were examined by western blotting. Cell Counting Kit‑8 and flow cytometry assays were used to detect the functional changes of RA‑FLSs transfected with UBD and MAPK inhibitor SB202190. The concentrations of inflammatory factors (IL‑2, IL‑6, IL‑10 and TNF‑α) were evaluated using ELISA kits. The results revealed that UBD was overexpressed in RA tissues compared with in the healthy control tissues. Functionally, UBD significantly accelerated the viability and proliferation of RA‑FLSs, whereas it inhibited their apoptosis. Furthermore, UBD significantly promoted the secretion of inflammatory factors (IL‑2, IL‑6, IL‑10 and TNF‑α). Mechanistically, elevated UBD activated phospohorylated‑p38 in RA‑FLSs. By contrast, UBD overexpression and treatment with the p38 MAPK inhibitor SB202190 not only partially relieved the UBD‑dependent effects on cell viability and proliferation, but also reversed its inhibitory effects on cell apoptosis. Furthermore, SB202190 partially inhibited the effects of UBD overexpression on the enhanced secretion of inflammatory factors. The present study indicated that UBD may mediate the activation of p38 MAPK, thereby facilitating the proliferation of RA‑FLSs and ultimately promoting the progression of RA. Therefore, UBD may be considered a potential therapeutic target and a promising prognostic biomarker for RA.
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February-2023
Volume 27 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Copy and paste a formatted citation
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Spandidos Publications style
Chen H, Tao L, Liang J, Pan C and Wei H: Ubiquitin D promotes the progression of rheumatoid arthritis via activation of the p38 MAPK pathway. Mol Med Rep 27: 53, 2023
APA
Chen, H., Tao, L., Liang, J., Pan, C., & Wei, H. (2023). Ubiquitin D promotes the progression of rheumatoid arthritis via activation of the p38 MAPK pathway. Molecular Medicine Reports, 27, 53. https://doi.org/10.3892/mmr.2023.12940
MLA
Chen, H., Tao, L., Liang, J., Pan, C., Wei, H."Ubiquitin D promotes the progression of rheumatoid arthritis via activation of the p38 MAPK pathway". Molecular Medicine Reports 27.2 (2023): 53.
Chicago
Chen, H., Tao, L., Liang, J., Pan, C., Wei, H."Ubiquitin D promotes the progression of rheumatoid arthritis via activation of the p38 MAPK pathway". Molecular Medicine Reports 27, no. 2 (2023): 53. https://doi.org/10.3892/mmr.2023.12940