ArticleArthritis research & therapy2009
Tumor necrosis factor alpha-induced adipose-related protein expression in experimental arthritis and in rheumatoid arthritis.
Article in Arthritis research & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 38 citations in OpenAlex.
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- Transcriptomic characterization of the human segmental endotoxin challenge model.Scientific reports · 2024Article
- The Role of STAMP2 in Pathogenesis of Chronic Diseases Focusing on Nonalcoholic Fatty Liver Disease: A Review.Biomedicines · 2022Review
- STEAP4 expression in CNS resident cells promotes Th17 cell-induced autoimmune encephalomyelitis.Journal of neuroinflammation · 2021Article
- STAMP2 Expression Mediated by Cytokines Attenuates Their Growth-Limiting Effects in Prostate Cancer Cells.Cancers · 2021Article
- The six-transmembrane protein Stamp2 ameliorates pulmonary vascular remodeling and pulmonary hypertension in mice.Basic research in cardiology · 2020Article
- Clinical and functional significance of STEAP4-splice variant in CD14Clinical and experimental immunology · 2018Article
- Dietary fat-associated osteoarthritic chondrocytes gain resistance to lipotoxicity through PKCK2/STAMP2/FSP27.Bone research · 2018Article
- TIARP attenuates autoantibody-mediated arthritis via the suppression of neutrophil migration by reducing CXCL2/CXCR2 and IL-6 expression.Scientific reports · 2016Article
- Specific overexpression of tumour necrosis factor-α-induced protein (TNFAIP)9 in CD14(+) CD16(-) monocytes in patients with rheumatoid arthritis: comparative analysis with TNFAIP3.Clinical and experimental immunology · 2015Article
- STEAP4 and insulin resistance.Endocrine · 2014Review
- STAMPing into Mitochondria.International journal of biological sciences · 2014Review
- Stamp2 controls macrophage inflammation through nicotinamide adenine dinucleotide phosphate homeostasis and protects against atherosclerosis.Cell metabolism · 2012Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTumor necrosis factor-alpha (TNFalpha) plays a pivotal role in rheumatoid arthritis (RA); however, the mechanism of action of TNFalpha antagonists in RA is poorly defined. Immunization of DBA/1 mice with glucose-6-phosphate isomerase (GPI) induces severe acute arthritis. This arthritis can be controlled by TNFalpha antagonists, suggesting similar etiology to RA. In this study, we explored TNFalpha-related mechanisms of arthritis.
methodsFirst, we performed GeneChip analysis using splenocytes of mice with GPI-induced arthritis. Expression of TNFalpha-induced adipose-related protein (TIARP) mRNA and protein in spleens, joints and lymph nodes was evaluated, and fluctuation of TIARP mRNA was analyzed after administration of anti-TNFalpha monoclonal antibody (mAb). Localization of TIARP in spleen and joints was also explored. Six-transmembrane epithelial antigen of the prostate (STEAP) families of proteins, the human ortholog of TIARP gene, were also evaluated in human peripheral blood mononucleocytes and synovium.
resultsAmong the arrayed TNFalpha-related genes, the expression of TIARP mRNA was the highest (more than 20 times the control). TIARP mRNA was detected specifically in joints and spleens of arthritic mice, and their levels in the synovia correlated with severity of joint swelling. Treatment with anti-TNF mAb significantly reduced TIARP mRNA expression in splenocytes. Among the splenocytes, CD11b+ cells were the main source of TIARP mRNA. Immunohistochemistry showed that TIARP protein was mainly localized in hyperplastic synovium. Among the STEAP family of proteins, STEAP4 was highly upregulated in joints of patients with RA and especially co-localized with CD68+ macrophages.
conclusionsThe results shed light on the new mechanism of action of TNFalpha antagonists in autoimmune arthritis, suggesting that TIARP plays an important role in inflammatory arthritis, through the regulation of inflammatory cytokines.
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