Blockade of translationally controlled tumor protein attenuated the aggressiveness of fibroblast-like synoviocytes and ameliorated collagen-induced arthritis.

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Abstrakt

Tytuł:: Blockade of translationally controlled tumor protein attenuated the aggressiveness of fibroblast-like synoviocytes and ameliorated collagen-induced arthritis.
Autorzy:: Kim M; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea.
Choe Y; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea.
Lee H; Graduate School of Pharmaceutical Sciences, College of Pharmacy, Ewha Womans University, Seoul, 03760, Republic of Korea.
Jeon MG; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea.
Park JH; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea.
Noh HS; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea.
Cheon YH; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea.
Park HJ; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea.
Park J; Department of Microbiology, Institute for Immunology and Immunological Disease, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.
Shin SJ; Department of Microbiology, Institute for Immunology and Immunological Disease, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.
Lee K; Graduate School of Pharmaceutical Sciences, College of Pharmacy, Ewha Womans University, Seoul, 03760, Republic of Korea. .
Lee SI; Department of Internal Medicine and Institute of Health Science, Gyeongsang National University School of Medicine and Hospital, Jinju, 52727, Republic of Korea. .
Źródło:: Experimental & molecular medicine [Exp Mol Med] 2021 Jan; Vol. 53 (1), pp. 67-80. Date of Electronic Publication: 2021 Jan 06.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: Jan. 2013- : New York : Nature Publishing Group
Original Publication: Seoul : Korean Society of Medical Biochemistry and Molecular Biology, 1996-
MeSH Terms:: Arthritis, Experimental/*metabolism
Arthritis, Rheumatoid/*metabolism
Fibroblasts/*metabolism
Synoviocytes/*metabolism
Tumor Protein, Translationally-Controlled 1/*metabolism
Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Arthritis, Experimental/drug therapy ; Arthritis, Rheumatoid/drug therapy ; Cells, Cultured ; Humans ; Mice ; Mice, Inbred C57BL ; Oligopeptides/pharmacology ; Oligopeptides/therapeutic use ; Protein Binding ; Tumor Protein, Translationally-Controlled 1/antagonists & inhibitors ; Tumor Protein, Translationally-Controlled 1/genetics
References:: Firestein, G. S. Evolving concepts of rheumatoid arthritis. Nature 423, 356–361 (2003). (PMID: 1274865510.1038/nature01661)
Blum, A. & Adawi, M. Rheumatoid arthritis (RA) and cardiovascular disease. Autoimmun. Rev. 18, 679–690 (2019). (PMID: 3105984010.1016/j.autrev.2019.05.005)
Cheon, Y. H. et al. The association of disease activity, pro-inflammatory cytokines, and neurotrophic factors with depression in patients with rheumatoid arthritis. Brain Behav. Immun. 73, 274–281 (2018). (PMID: 2978785610.1016/j.bbi.2018.05.012)
De Cock, D. & Hyrich, K. Malignancy and rheumatoid arthritis: epidemiology, risk factors and management. Best. Pr. Res Clin. Rheumatol. 32, 869–886 (2018). (PMID: 10.1016/j.berh.2019.03.011)
Singh, J. A. et al. 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Rheumatol. 68, 1–26 (2016). (PMID: 26545940)
Favalli, E. G. et al. Twelve-year retention rate of first-line tumor necrosis factor inhibitors in rheumatoid arthritis: real-life data from a local registry. Arthritis Care Res (Hoboken) 68, 432–439 (2016). (PMID: 10.1002/acr.22788)
Rutherford, A. I., Subesinghe, S., Hyrich, K. L. & Galloway, J. B. Serious infection across biologic-treated patients with rheumatoid arthritis: results from the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis. Ann. Rheum. Dis. 77, 905–910 (2018). (PMID: 29592917)
Mankia, K. & Emery, P. Preclinical rheumatoid arthritis: progress toward prevention. Arthritis Rheumatol. 68, 779–788 (2016). (PMID: 2681467710.1002/art.39603)
van Steenbergen, H. W., da Silva, J. A. P., Huizinga, T. W. J. & van der Helm-van Mil, A. H. M. Preventing progression from arthralgia to arthritis: targeting the right patients. Nat. Rev. Rheumatol. 14, 32–41 (2018).
Orr, C. et al. Synovial tissue research: a state-of-the-art review. Nat. Rev. Rheumatol. 13, 630 (2017). (PMID: 2893594510.1038/nrrheum.2017.161)
You, S., Koh, J. H., Leng, L., Kim, W. U. & Bucala, R. The tumor-like phenotype of rheumatoid synovium: molecular profiling and prospects for precision medicine. Arthritis Rheumatol. 70, 637–652 (2018). (PMID: 29287304592071310.1002/art.40406)
Bottini, N. & Firestein, G. S. Duality of fibroblast-like synoviocytes in RA: passive responders and imprinted aggressors. Nat. Rev. Rheumatol. 9, 24–33 (2013). (PMID: 2314789610.1038/nrrheum.2012.190)
Lefevre, S. et al. Synovial fibroblasts spread rheumatoid arthritis to unaffected joints. Nat. Med. 15, 1414–1420 (2009). (PMID: 19898488367835410.1038/nm.2050)
Bucala, R., Ritchlin, C., Winchester, R. & Cerami, A. Constitutive production of inflammatory and mitogenic cytokines by rheumatoid synovial fibroblasts. J. Exp. Med 173, 569–574 (1991). (PMID: 199764710.1084/jem.173.3.569)
Pitzalis, C., Kelly, S. & Humby, F. New learnings on the pathophysiology of RA from synovial biopsies. Curr. Opin. Rheumatol. 25, 334–344 (2013). (PMID: 2349274010.1097/BOR.0b013e32835fd8eb)
Noss, E. H. & Brenner, M. B. The role and therapeutic implications of fibroblast-like synoviocytes in inflammation and cartilage erosion in rheumatoid arthritis. Immunol. Rev. 223, 252–270 (2008). (PMID: 1861384110.1111/j.1600-065X.2008.00648.x)
Lee, H. S. et al. Regulation of apoptosis and inflammatory responses by insulin-like growth factor binding protein 3 in fibroblast-like synoviocytes and experimental animal models of rheumatoid arthritis. Arthritis Rheumatol. 66, 863–873 (2014). (PMID: 2475713910.1002/art.38303)
Hah, Y. S. et al. A20 suppresses inflammatory responses and bone destruction in human fibroblast-like synoviocytes and in mice with collagen-induced arthritis. Arthritis Rheum. 62, 2313–2321 (2010). (PMID: 2050622110.1002/art.27545)
Yenofsky, R., Cereghini, S., Krowczynska, A. & Brawerman, G. Regulation of mRNA utilization in mouse erythroleukemia cells induced to differentiate by exposure to dimethyl sulfoxide. Mol. Cell Biol. 3, 1197–1203 (1983). (PMID: 657728037011010.1128/MCB.3.7.1197)
Chitpatima, S. T., Makrides, S., Bandyopadhyay, R. & Brawerman, G. Nucleotide sequence of a major messenger RNA for a 21 kilodalton polypeptide that is under translational control in mouse tumor cells. Nucleic Acids Res 16, 2350 (1988). (PMID: 335779233823710.1093/nar/16.5.2350)
Warner, J. A., Pienkowski, M. M., Plaut, M., Norman, P. S. & Lichtenstein, L. M. Identification of histamine releasing factor(s) in the late phase of cutaneous IgE-mediated reactions. J. Immunol. 136, 2583–2587 (1986). (PMID: 2419443)
Yoneda, K. et al. Stimulation of human bronchial epithelial cells by IgE-dependent histamine-releasing factor. Am. J. Physiol. Lung Cell Mol. Physiol. 286, L174–L181 (2004). (PMID: 1294893410.1152/ajplung.00118.2003)
Sampson, H. A., Broadbent, K. R. & Bernhisel-Broadbent, J. Spontaneous release of histamine from basophils and histamine-releasing factor in patients with atopic dermatitis and food hypersensitivity. N. Engl. J. Med 321, 228–232 (1989). (PMID: 247340010.1056/NEJM198907273210405)
Rho, S. B. et al. Anti-apoptotic protein TCTP controls the stability of the tumor suppressor p53. FEBS Lett. 585, 29–35 (2011). (PMID: 2108112610.1016/j.febslet.2010.11.014)
Bae, S. Y., Kim, H. J., Lee, K. J. & Lee, K. Translationally controlled tumor protein induces epithelial to mesenchymal transition and promotes cell migration, invasion and metastasis. Sci. Rep. 5, 8061 (2015). (PMID: 25622969430696310.1038/srep08061)
Acunzo, J., Baylot, V., So, A. & Rocchi, P. TCTP as therapeutic target in cancers. Cancer Treat. Rev. 40, 760–769 (2014). (PMID: 2465092710.1016/j.ctrv.2014.02.007)
Maslinska, D. et al. Histamine releasing factor (HRF) in pannus of joints affected by rheumatoid arthritis. Inflamm. Res 57, S61–S62 (2008). (PMID: 1834548810.1007/s00011-007-0630-2)
Aletaha, D. et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 62, 2569–2581 (2010). (PMID: 2087259510.1002/art.27584)
Fransen, J. & van Riel, P. L. The disease activity score and the EULAR response criteria. Rheum. Dis. Clin. North Am. 35, 745–757 (2009). (PMID: 1996261910.1016/j.rdc.2009.10.001)
Altman, R. et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum. 29, 1039–1049 (1986). (PMID: 374151510.1002/art.1780290816)
van der Linden, S., Valkenburg, H. A. & Cats, A. Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria. Arthritis Rheum. 27, 361–368 (1984). (PMID: 623193310.1002/art.1780270401)
Criteria for diagnosis of Behcet’s disease. International Study Group for Behcet’s Disease. Lancet 335, 1078-1080 (1990).
Woo, S. J. et al. Myeloid deletion of SIRT1 suppresses collagen-induced arthritis in mice by modulating dendritic cell maturation. Exp. Mol. Med. 48, e221 (2016). (PMID: 26987484489287710.1038/emm.2015.124)
Woo, S. J. et al. Myeloid sirtuin 6 deficiency accelerates experimental rheumatoid arthritis by enhancing macrophage activation and infiltration into synovium. EBioMedicine 38, 228–237 (2018). (PMID: 30429089630634710.1016/j.ebiom.2018.11.005)
Chen, S. H. et al. A knockout mouse approach reveals that TCTP functions as an essential factor for cell proliferation and survival in a tissue- or cell type-specific manner. Mol. Biol. Cell 18, 2525–2532 (2007). (PMID: 17475776192481810.1091/mbc.e07-02-0188)
Kim, M. et al. Dimerization of translationally controlled tumor protein is essential for its cytokine-like activity. PLoS ONE 4, e6464 (2009). (PMID: 19649253271510110.1371/journal.pone.0006464)
Jeon, M. G. et al. Suppressive effects of TSAHC in an Experimental mouse model and fibroblast-like synoviocytes of rheumatoid arthritis. Inflammation 40, 1825–1835 (2017). (PMID: 2881970110.1007/s10753-017-0621-6)
Kim, W. S. et al. Mycobacterium tuberculosis Rv3628 drives Th1-type T cell immunity via TLR2-mediated activation of dendritic cells and displays vaccine potential against the hyper-virulent Beijing K strain. Oncotarget 7, 24962–24982 (2016). (PMID: 27097115504188310.18632/oncotarget.8771)
Kim, M., Maeng, J. & Lee, K. Dimerization of TCTP and its clinical implications for allergy. Biochimie 95, 659–666 (2013). (PMID: 2310426810.1016/j.biochi.2012.10.007)
Maslinska, D., Gujski, M., Laure-Kamionowska, M., Szukiewicz, D. & Wojtecka-Lukasik, E. Subcellular localization of histamine in articular cartilage chondrocytes of rheumatoid arthritis patients. Inflamm. Res 53, S35–S36 (2004). (PMID: 1505460710.1007/s00011-003-0316-3)
Malone, D. G., Irani, A. M., Schwartz, L. B., Barrett, K. E. & Metcalfe, D. D. Mast cell numbers and histamine levels in synovial fluids from patients with diverse arthritides. Arthritis Rheum. 29, 956–963 (1986). (PMID: 242709310.1002/art.1780290803)
Woolley, D. E. The mast cell in inflammatory arthritis. N. Engl. J. Med 348, 1709–1711 (2003). (PMID: 1271174810.1056/NEJMcibr023206)
Adlesic, M. et al. Histamine in rheumatoid arthritis. Scand. J. Immunol. 65, 530–537 (2007). (PMID: 1752394510.1111/j.1365-3083.2007.01938.x)
Cowden, J. M. et al. The histamine H4 receptor mediates inflammation and Th17 responses in preclinical models of arthritis. Ann. Rheum. Dis. 73, 600–608 (2014). (PMID: 2412645610.1136/annrheumdis-2013-203832)
Thurmond, R. L. et al. Toreforant, a histamine h4 receptor antagonist, in patients with active rheumatoid arthritis despite methotrexate therapy: results of 2 phase II studies. J. Rheumatol. 43, 1637–1642 (2016). (PMID: 2742289110.3899/jrheum.160164)
Boyle, D. L. et al. Toreforant, an orally active histamine H4-receptor antagonist, in patients with active rheumatoid arthritis despite methotrexate: mechanism of action results from a phase 2, multicenter, randomized, double-blind, placebo-controlled synovial biopsy study. Inflamm. Res. 68, 261–274 (2019). (PMID: 3073913010.1007/s00011-019-01218-y)
Hammaker, D. & Firestein, G. S. Go upstream, young man”: lessons learned from the p38 saga. Ann. Rheum. Dis. 69, i77–i82 (2010). (PMID: 19995751291101610.1136/ard.2009.119479)
Thueson, D. O., Speck, L. S., Lett-Brown, M. A. & Grant, J. A. Histamine-releasing activity (HRA). I. Production by mitogen- or antigen-stimulated human mononuclear cells. J. Immunol. 123, 626–632 (1979). (PMID: 88479)
Dekkers, J. S., Schoones, J. W., Huizinga, T. W., Toes, R. E. & van der Helm-van Mil, A. H. Possibilities for preventive treatment in rheumatoid arthritis? Lessons from experimental animal models of arthritis: a systematic literature review and meta-analysis. Ann. Rheum. Dis. 76, 458–467 (2017).
Bevaart, L., Vervoordeldonk, M. J. & Tak, P. P. Evaluation of therapeutic targets in animal models of arthritis: how does it relate to rheumatoid arthritis? Arthritis Rheum. 62, 2192–2205 (2010). (PMID: 2050632210.1002/art.27503)
Hegen, M., Keith, J. C. Jr, Collins, M. & Nickerson-Nutter, C. L. Utility of animal models for identification of potential therapeutics for rheumatoid arthritis. Ann. Rheum. Dis. 67, 1505–1515 (2008). (PMID: 1805547410.1136/ard.2007.076430)
Substance Nomenclature:: 0 (Anti-Inflammatory Agents)
0 (Oligopeptides)
0 (Tpt1 protein, mouse)
0 (Tumor Protein, Translationally-Controlled 1)
Entry Date(s):: Date Created: 20210107 Date Completed: 20220215 Latest Revision: 20230127
Update Code:: 20240105
PubMed Central ID:: PMC8080778
DOI:: 10.1038/s12276-020-00546-y
PMID:: 33408335
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Histamine releasing factor/translationally controlled tumor protein (HRF/TCTP) stimulates cancer progression and allergic responses, but the role of HRF/TCTP in rheumatoid arthritis (RA) remains undefined. In this study, we explored the pathogenic significance of HRF/TCTP and evaluated the therapeutic effects of HRF/TCTP blockade in RA. HRF/TCTP transgenic (TG) and knockdown (KD) mice with collagen-induced arthritis (CIA) were used to determine the experimental phenotypes of RA. HRF/TCTP levels in the sera of RA patients were measured and compared to those from patients with osteoarthritis (OA), ankylosing spondylitis, Behçet's disease, and healthy controls. HRF/TCTP expression was also assessed in the synovium and fibroblast-like synoviocytes (FLSs) obtained from RA or OA patients. Finally, we assessed the effects of HRF/TCTP and dimerized HRF/TCTP-binding peptide-2 (dTBP2), an HRF/TCTP inhibitor, in RA-FLSs and CIA mice. Our clinical, radiological, histological, and biochemical analyses indicate that inflammatory responses and joint destruction were increased in HRF/TCTP TG mice and decreased in KD mice compared to wild-type littermates. HRF/TCTP levels in the sera, synovial fluid, synovium, and FLSs were higher in patients with RA than in control groups. Serum levels of HRF/TCTP correlated well with RA disease activity. The tumor-like aggressiveness of RA-FLSs was exacerbated by HRF/TCTP stimulation and ameliorated by dTBP2 treatment. dTBP2 exerted protective and therapeutic effects in CIA mice and had no detrimental effects in a murine tuberculosis model. Our results indicate that HRF/TCTP is a novel biomarker and therapeutic target for the diagnosis and treatment of RA.

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