|
|
|
| Research progress on the correlation between high mobility group box chromosomal protein l and rheumatoid arthritis |
| LIU Wei1* HUANG Jian1* CHEN Caixia2 WANG Dan3 |
1.Department of Joint Surgery, the Second Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Hohhot 010010, China; 2.Clinical Medical Research Center, Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Hohhot 010010, China;
3.Geriatric Medical Center, Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Hohhot 010010, China |
|
|
|
Abstract Rheumatoid arthritis is a chronic non-specific inflammatory disease of the joint synovium with joint lesions as the main manifestation, and the course of disease is progressive. High mobility group box chromosomal protein 1 is involved in the evolution and progression of various autoimmune diseases as a potential inflammation-inducing factor. And the abnormal expression of high mobility group box chromosomal protein 1 is closely related to the occurrence and development of rheumatoid arthritis. This article further elaborates and demonstrates that the expression of high mobility group box chromosomal protein 1 in serum of patients with rheumatoid arthritis promotes the up-regulation of inflammatory factor-related receptors, but its correlation with clinical indicators is still unclear. The expression of high mobility group box chromosomal protein 1 in synovial membrane in patients with rheumatoid arthritis promotes synovial inflammatory expression. High mobility group box chromosomal protein 1 promotes the synthesis and release of inflammatory cytokines, pathological proliferation, apoptosis, autophagy and irreversible progression of phenotypic transformation in synovial fibroblasts in rheumatoid arthritis. In theory, it provides a new target for the clinical diagnosis and disease intervention of rheumatoid arthritis.
|
|
|
|
|
|
[1] Andersson U，Wang H，Palmblad K，et al. High mobility group 1 protein（HMG-1）stimulates proinflammatory cytokine synthesis in human monocytes [J]. J Exp Med，2000， 192（4）：565-570.
[2] Cacciapaglia F，Anelli MG，Rizzo D，et al. Influence of TNF-alpha inhibition on oxidative stress of rheumatoid arthritis patients [J]. Reumatismo，2015，67（3）：97-102.
[3] 朱力.HMGB1-LPS介导的自噬/凋亡失衡在类风湿关节炎滑膜成纤维细胞致病理损伤中的作用和机制[D].上海：第二军医大学，2016.
[4] 梁树芬，张娜，游锦梅，等.高迁移率族蛋白B1在类风湿关节炎发病中的作用研究[J].中国药物与临床，2017，17（9）：1329-1331.
[5] Motomura H，Matsushita I，Seki E，et al. Inhibitory effect of tacrolimus on progression of joint damage in patients with rheumatoid arthritis [J]. Int J Rheum Dis，2014，17（7）：749-754.
[6] Komatsu N，Okamoto K，Sawa S，et al. Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis [J]. Nat Med，2014，20（1）：62-68.
[7] Komatsu N，Takayanagi H. Arthritogenic T cells in autoimmune arthritis [J]. Int J Biochem Cell Biol，2015，58：92-96.
[8] Burmester GR，Feist E，Dorner T. Emerging cell and cytokine targets in rheumatoid arthritis [J]. Nat Rev Rheumatol，2014，10（2）：77-88.
[9] Selaas O，Nordal HH，Halse AK，et al. Serum Markers in Rheumatoid Arthritis：A Longitudinal Study of Patients Undergoing Infliximab Treatment [J]. Int J Rheumatol，2015，2015：276815.
[10] Zhang HC，Liu MX，Wang EP，et al. Effect of sinomenine on the expression of rheumatoid arthritis fibroblast-like synoviocytes MyD88 and TRAF6 [J]. Genet Mol Res，2015， 14（4）：18928-18935.
[11] 陈岩.HMGB1-LPS复合物促进滑膜成纤维细胞向类风湿关节炎滑膜成纤维细胞表型的转变[D].上海：第二军医大学，2013.
[12] 贺诤雯.HMGB1与LPS协同激活类风湿性关节炎滑膜成纤维细胞产生基质金属蛋白酶的分子机制[D].上海：第二军医大学，2011.
[13] He ZW，Qin YH，Wang ZW，et al. HMGB1 acts in synergy with lipopolysaccharide in activating rheumatoid synovial fibroblasts via p38 MAPK and NF-kappaB signaling pathways [J]. Mediators Inflamm，2013，2013：596716.
[14] Koszarny A，Majdan M，Suszek D，et al. Autoantibodies against gliadin in rheumatoid arthritis and primary Sjogren′s syndrome patients [J]. Wiad Lek，2015，68（3）：242-247.
[15] Araki Y，Aizaki Y，Sato K，et al. Altered gene expression profiles of histone lysine methyltransferases and demethylases in rheumatoid arthritis synovial fibroblasts [J]. Clin Exp Rheumatol，2018，36（2）：314-316.
[16] Büyüktimkin B，Kiptoo P，Siahaan TJ. Bifunctional Peptide Inhibitors Suppress Interleukin-6 Proliferation and Ameliorates Murine Collagen-Induced Arthritis [J]. J Clin Cell Immunol，2014，5（6）.
[17] Mathew AJ，Ravindran V. Infections and arthritis [J]. Best Pract Res Clin Rheumatol，2014，28（6）：935-959.
[18] Cutolo M，Spies CM，Buttgereit F，et al. The supplementary therapeutic DMARD role of low-dose glucocorticoids in rheumatoid arthritis [J]. Arthritis Res Ther，2014， 16 Suppl 2：S1.
[19] Yang H，Tracey KJ. High mobility group box 1（HMGB1）[J]. Critical Care Medicine，2005，33（12 Suppl）：S472-S474.
[20] Taniguchi N，Kawahara K，Yone K. High mobility group box chromosomal protein plays a role in the pathogenesis of rheumatoid arthritis as a novel cytosine [J]. Arthritis Rheum，2003，48：971-981.
[21] Calogero S，Grassi F，Aguzzi A，et al. The lack of chromosomal protein Hmg1 does not disrupt cell growth but causes lethal hypoglycaemia in newborn mice [J]. Nat Genet，1999，22（3）：276-280.
[22] Kokkola R，Li J，Sundberg E，et al. Successful treatment of collagen-induced arthritis in mice and rats by targeting extracellular high mobility group box chromosomal protein 1 activity [J]. Arthritis Rheum，2003，48（7）：2052-2058.
[23] Bianchi ME，Beltrame M. Upwardly mobile proteins. Workshop： the role of HMG proteins in chromatin structure，gene expression and neoplasia [J]. EMBO Rep，2000，1（2）：109-114.
[24] Hreggvidsdottir HS，Ostberg T，W?覿h?覿maa H，et al. The alarmin HMGB1 acts in synergy with endogenous and exogenous danger signals to promote inflammation [J]. J Leukoc Biol，2009，86（3）：655-662.
[25] Youn JH，Oh YJ，Kim ES，et al. High mobility group box 1 protein binding to lipopolysaccharide facilitates transfer of lipopolysaccharide to CD14 and enhances lipop-olysaccharide-mediated TNF-alpha production in human monocytes [J]. J Immunol，2008，180（7）：5067-5074.
[26] Goldstein RS. High mobility group box-1 protein as a tumor necrosis factor-independent therapeutic target in rheumatoid arthritis [J]. Arthritis Res Ther，2008，10（3）：111.
[27] Yang H，Wang H，Chavan SS，et al. High Mobility Group Box Protein 1（HMGB1）：The Prototypical Endogenous Danger Molecule [J]. Mol Med，2015，21 Suppl 1：S6-S12.
[28] Shi Y，Sandoghchian Shotorbani S，Su Z，et al. Enhanced HMGB1 expression may contribute to Th17 cells activation in rheumatoid arthritis [J]. Clin Dev Immunol，2012， 2012：295081.
[29] Qin Y，Chen Y，Wang W，et al. HMGB1-LPS complex promotes transformation of osteoarthritis synovial fibroblasts to a rheumatoid arthritis synovial fibroblast-like phenotype [J]. Cell Death Dis，2014，5：e1 077.
[30] Park JS，Svetkauskaite D，He Q，et al. Involvement of toll-like receptors 2 and 4 in cellular activation by high mobility group box 1 protein [J]. J Biol Chem，2004，279（9）：7370-7377.
[31] Fiuza C，Bustin M，Talwar S，et al. Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells [J]. Blood，2003，101（7）：2652-2660.
[32] Rendon-Mitchell B，Ochani M，Li J，et al. IFN-gamma induces high mobility group box 1 protein release partly through a TNF-dependent mechanism [J]. J Immunol，2003，170（7）：3890-3897.
[33] Scaffidi P，Misteli T，Bianchi ME. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation [J]. Nature，2002，418（6894）：191-195.
[34] Lei C，Wu B，Cao T，et al. Activation of the high-mobility group box 1 protein-receptor for advanced glycation end-products signaling pathway in rats during neurogenesis after intracerebral hemorrhage [J]. Stroke，2015，46（2）：500-506.
[35] Ozturk N，Singh I，Mehta A，et al. HMGA proteins as modulators of chromatin structure during transcriptional activation [J]. Front Cell Dev Biol，2014，2：5.
[36] 刘小军，茹晋丽，赵华明，等.血清高迁移率族蛋白1水平与类风湿关节炎临床指标的相关性[J].中华临床免疫和变态反应杂志，2010，4（3）：201-204.
[37] 郭惠芳，刘淑霞，刘晓雷，等.高迁移率族蛋白1及Toll样受体4在类风湿关节炎患者血清和外周血单个核细胞中的表达及意义[J].中华风湿病学杂志，2009，13（5）：333-336.
[38] 殷春兰，黄新翔，王俊祥，等.类风湿关节炎患者高迁移率族蛋白1的检测及临床意义[J].北京医学，2011，33（7）：551，554.
[39] 何蛟，贾治林.类风湿关节炎患者血清HMGB1及TGF-1的表达及意义[J].大连医科大学学报，2015，37（2）：148-150.
[40] 郭惠芳，刘淑霞，马丽艳，等.类风湿关节炎患者血清中高迁移率族蛋白1的作用及其与MMP2、TIMP2的关系[J].中国现代医学杂志，2010，20（2）：192-195.
[41] 贾瑛，郑健.类风湿性关节炎患者血清HMGB1水平与其他炎性因子的相关性[J].陕西医学杂志，2011，40（3）：296-297，301.
[42] 左晓霞，周亚欧，龚艳晖，等.类风湿关节炎患者外周血高迁移率族蛋白1表达[J].中华内科杂志，2007，46（7）：547-550.
[43] 徐力，刘晶.HMGB1在评价类风湿关节炎疾病活动度中的意义及与RA-ILD关系初探[J].风湿病与关节炎，2015，4（4）：10-12，19.
[44] 米亚英，杨丽丽，孙利平.HMGB1及TLR2_TLR4在类风湿关节炎中的表达及意义[J].基础医学与临床，2013， 33（4）：476-479.
[45] Kim HY，Park SY，Lee SW，et al. Inhibition of HMGB1-induced angiogenesis by cilostazol via SIRT1 activation in synovial fibroblasts from rheumatoid arthritis [J]. PLoS One，2014，9（8）：e104743.
[46] Kaur PP，Derk CT，Chatterji M，et al. Septic arthritis caused by Actinobacillus ureae in a patient with rheumatoid arthritis receiving anti-tumor necrosis factor-alpha therapy [J]. J Rheumatol，2004，31（8）：1663-1665.
[47] 郭惠芳，孙熠峰，刘淑霞，等.HMGB1在类风湿关节炎疾病活动中的作用及其与EMMPRIN/CD147表达的相关性研 [J]. 实用临床免疫学，2009，25（7）：662-665.
[48] Kokkola R，Sundberg E，Ulfgren AK，et al. High mobility group box chromosomal protein 1： a novel proinflammatory mediator in synovitis [J]. Arthritis Rheum，2002，46（10）：2598-2603.
[49] 郑毅，董馨，陆江阳.类风湿关节炎滑膜中高迁移率族蛋白1的表达[J].中华风湿病学杂志，2005，9（11）：684-686.
[50] Andersson U，Antoine DJ，Tracey KJ. The functions of HMGB1 depend on molecular localization and post-translational modifications [J]. J Intern Med，2014，276（5）：420-424.
[51] 龚震.HMGB1对RA患者成纤维样滑膜细胞增殖及IL-6、IL-8、MMP-3表达的影响[D].长沙：中南大学，2011.
[52] 贺诤雯，戴生明，秦阳华，等.HMGB1促进类风湿性关节炎滑膜成纤维细胞表达基质金属蛋白酶-13[J].临床免疫学，2011，27（12）：1097-1100.
[53] Kato M，Ospelt C，Gay RE，et al. Dual role of autophagy in stress-induced cell death in rheumatoid arthritis synovial fibroblasts [J]. Arthritis Rheumatol，2014，66（1）：40-48.
[54] Connor AM，Mahomed N，Gandhi R，et al. TNF-α modulates protein degradation pathways in rheumatoid arthritis synovial fibroblasts [J]. Arthritis Res Ther，2012，14（2）：R62.
[55] Shin YJ，Han SH，Kim DS，et al. Autophagy induction and CHOP under-expression promotes survival of fibroblasts from rheumatoid arthritis patients under endoplasmic reticulum stress [J]. Arthritis Res Ther，2010，12（1）：R19.
[56] Xu JK，Hiroshi K，Zheng JJ，et al. Protective effect of tanshinones against liver injury in mice loaded with restraint stress [J]. Yao Xue Xue Bao. 2006，41（7）：631-635.
[57] Musumeci G，Castrogiovanni P，Trovato FM，et al. Biomarkers of Chondrocyte Apoptosis and Autophagy in Osteoarthritis [J]. Int J Mol Sci，2015，16（9）：20 560-20 575.
[58] Schuster C，Gerold KD，Schober K，et al. The Autoimmunity-Associated Gene CLEC16A Modulates Thymic Epithelial Cell Autophagy and Alters T Cell Selection [J]. Immunity，2015，42（5）：942-952.
[59] Yin G，Wang Y，Cen XM，et al. Lipid peroxidation-mediated inflammation promotes cell apoptosis through activation of NF-kappaB pathway in rheumatoid arthritis synovial cells [J]. Mediators Inflamm，2015，2015：460 310.
[60] Levine B，Mizushima N，Virgin HW. Autophagy in immunity and inflammation [J]. Nature，2011，469（7330）：323-335.
[61] Lotz MK，Caramés B. Autophagy and cartilage homeostasis mechanisms in joint health，aging and OA [J]. Nat Rev Rheumatol，2011，7（10）：579-587. |
|
|
|
