ArticleClinical rheumatology2018
Thioredoxin 1 is associated with the proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocytes.
Article in Clinical rheumatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Identification and experimental validation of CD74, PGLYRP1, and TXN as potential biomarkers in rheumatoid arthritis: an integrative bulk and ScRNA-seq study.Frontiers in immunology · 2026Article
- Revealing Metabolic Reprogramming Genes as Biomarkers of Rheumatoid Arthritis: A Bioinformatics Study Based on Ensemble Learning Approach and Single Cell RNA Sequencing.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Geranylgeranylacetone Ameliorates Skin Inflammation by Regulating and Inducing Thioredoxin via the Thioredoxin Redox System.Antioxidants (Basel, Switzerland) · 2023Article
- Disequilibrium in the Thioredoxin Reductase-1/Thioredoxin-1 Redox Couple Is Associated with Increased T-Cell Apoptosis in Children with Autism.Metabolites · 2023Article
- Comprehensive ceRNA network for MACF1 regulates osteoblast proliferation.BMC genomics · 2022Article
- Molecular Mechanism Investigation on Monomer Kaempferol of the Traditional Medicine Dingqing Tablet in Promoting Apoptosis of Acute Myeloid Leukemia HL-60 Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Compensatory Protection of Thioredoxin-Deficient Cells from Etoposide-Induced Cell Death by Selenoprotein W via Interaction with 14-3-3.International journal of molecular sciences · 2021Article
- Hsa_circ_0032131 knockdown inhibits osteoarthritis progression via the miR-502-5p/PRDX3 axis.Aging · 2021Article
- Lipoxin A4-Mediated p38 MAPK Signaling Pathway Protects Mice Against Collagen-Induced Arthritis.Biochemical genetics · 2021Article
- Reverse Microbiomics: A New Reverse Dysbiosis Analysis Strategy and Its Usage in Prediction of Autoantigens and Virulent Factors in Dysbiotic Gut Microbiomes From Rheumatoid Arthritis Patients.Frontiers in microbiology · 2021Article
- The impact of thioredoxin reduction of allosteric disulfide bonds on the therapeutic potential of monoclonal antibodies.The Journal of biological chemistry · 2019Article
- Manganese dioxide nanoparticles protect cartilage from inflammation-induced oxidative stress.Biomaterials · 2019Article
- An interplay of structure and intrinsic disorder in the functionality of peptidylarginine deiminases, a family of key autoimmunity-related enzymes.Cellular and molecular life sciences : CMLS · 2019Review
- Investigation of gene expression profiles in a rat adjuvant arthritis model suggests an effective role of triptolide via PI3K-AKT signaling.Experimental and therapeutic medicine · 2019Article
- Thioredoxin Modulates Protein Arginine Deiminase 4 (PAD4)-Catalyzed Citrullination.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
We aimed to investigate the possible effects of thioredoxin 1 (Trx1) on the proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) and elucidate the possible mechanisms involved. We investigated the distribution and expression of Trx1 in synovial tissues from RA and osteoarthritis (OA) patients by immunohistochemistry and real-time polymerase chain reaction (RT-PCR) analyses. RA-FLSs were isolated and cultured under normoxic (21% oxygen) or hypoxic (3% oxygen) concentrations. Transfection of Trx1-siRNAs and a Trx1 overexpression construct was conducted to manipulate the expression of Trx1. Protein expression was detected by Western blot. Doxorubicin (Adriamycin, ADR) was used to induce apoptosis. LY-294002 was used for the inhibition of PI3K-Akt. Cell proliferation and apoptosis were determined by MTS (3-[4,5-dimethylthiazol-2-yl]-5-[3-carboxymethoxyphenyl]-2-[4-sulfophenyl]-2H-tetrazolium, inner salt) assay and flow cytometry, respectively. The mRNA and protein expression of Trx1 in RA tissues was higher than that in OA tissues. The expression levels of Trx1 and cell proliferation in RA-FLSs were increased under hypoxia in comparison to those under normoxia. In hypoxia, downregulation of Trx1 significantly suppressed FLS proliferation, and the expression of PI3Kp85, phospho-Akt, and Bcl-2, while notably increased FLS apoptosis and the expression of active Caspase3 and Bax. In normoxia, Trx1 overexpression promoted the FLS proliferation and the expression of PI3Kp85, phospho-Akt, and Bcl-2, but inhibited FLS apoptosis and the expression of active Caspase3 and Bax in FLSs. Such effects were partially repressed by LY-294002 treatment. Trx1 may play an important role in regulating the proliferation and apoptosis of RA-FLSs by modulating PI3K-Akt activation.
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