ArticleExperimental and therapeutic medicine2018
HOXD10 silencing suppresses human fibroblast-like synoviocyte migration in rheumatoid arthritis via downregulation of the p38/JNK pathway.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Correlation of fecal microbiome dysregulation to synovial transcriptome in an equine model of obesity associated osteoarthritis.Annals of translational medicine · 2024Article
- Joint-specific regulation of homeobox D10 expression in rheumatoid arthritis fibroblast-like synoviocytes.PloS one · 2024Article
- HOXD10 regulates intestinal permeability and inhibits inflammation of dextran sulfate sodium-induced ulcerative colitis through the inactivation of the Rho/ROCK/MMPs axis.Open medicine (Warsaw, Poland) · 2024Article
- Comparative computational analysis to distinguish mesenchymal stem cells from fibroblasts.Frontiers in immunology · 2023Article
- Specialized Pro-Resolving Mediators Do Not Inhibit the Synthesis of Inflammatory Mediators Induced by Tumor Necrosis Factor-α in Synovial Fibroblasts.Yonago acta medica · 2022Article
- Macroautophagy in lymphatic endothelial cells inhibits T cell-mediated autoimmunity.The Journal of experimental medicine · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Homeobox D10 (HOXD10) belongs to the human homeobox (HOX) gene family, and the homologous protein encoded by HOX primarily controls cell differentiation and morphogenesis during embryonic development. The current study aimed to explore the roles and mechanisms of HOXD10 in the migration of human fibroblast-like synoviocytes in rheumatoid arthritis (RAFLS). Cell counting kit-8, cell migration and wound healing assays were performed to examine the cell viability and migration, respectively. Western blot and reverse transcription-quantitative polymerase chain reaction assays were used to evaluate the association between mRNA and protein expression levels. The results revealed HOXD10 expression was upregulated in tissues from patients with RA. HOXD10 silencing inhibited the viability of RAFLS. In addition, HOXD10 silencing suppressed the migration of RAFLS through modulating the expression of cadherin-11, N-cadherin, E-cadherin, vimentin, zonula occludens-1, integrinβ1 and paxillin. In conclusion, HOXD10 silencing downregulates the p38/c-Jun N-terminal kinase signaling pathway, which in turn may suppress the migration of RAFLS.
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