国际口腔医学杂志

国际口腔医学杂志 ›› 2020, Vol. 47 ›› Issue (5): 607-615.doi: 10.7518/gjkq.2020022

• 综述 • 上一篇    下一篇

微小RNA 155对骨免疫的调控及其在牙周炎中作用的研究进展

孙坚炜(),雷利红,谭静怡,陈莉丽()   

  1. 浙江大学医学院附属第二医院牙周科 杭州 310009
  • 收稿日期:2019-11-30 修回日期:2020-03-25 出版日期:2020-09-01 发布日期:2020-09-16
  • 通讯作者: 陈莉丽
  • 作者简介:孙坚炜,硕士,Email: 21818178@zju.edu.cn
  • 基金资助:
    国家自然科学基金(81771072);浙江省科技计划项目(2017C33141)

Regulation of osteoimmunology by MicroRNA 155 and research progress of its possible mechanism in periodontitis

Sun Jianwei(),Lei Lihong,Tan Jingyi,Chen Lili()   

  1. Dept. of Periodontics, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China
  • Received:2019-11-30 Revised:2020-03-25 Online:2020-09-01 Published:2020-09-16
  • Contact: Lili Chen
  • Supported by:
    National Natural Science Foundation of China(81771072);the Science and Technology Program of Zhejiang Province(2017C33141)

RichHTML

16

PDF (PC)

114

摘要：

牙周炎是以牙龈炎症和牙槽骨进行性破坏为特征的慢性感染性疾病,牙周菌斑微生物和宿主免疫反应之间的相互作用影响着疾病的过程和进展。骨免疫学作为一个新的交叉学科领域,主要研究骨骼系统和免疫系统之间的分子交互机制,与牙周炎的发生密切相关。微小RNA 155（miR-155）是一种真核生物内源性非编码RNA,可与目标基因mRNA的3’-非编码区结合而抑制其表达,参与机体的免疫、造血、炎症等生理或病理过程。大量研究表明,在牙周炎发展过程中miR-155的表达量发生改变,但目前文献报道的结果尚不一致,且miR-155还可通过多条途径参与骨骼系统的调控。本文对miR-155在骨免疫及牙周炎发生中的调节作用进行综述,以期为牙周炎的临床治疗提供新的思路和策略。

关键词: 微小RNA, 骨免疫, 牙周炎, 骨代谢, 成骨细胞, 破骨细胞

Abstract:

Periodontitis is a chronic infectious disease that is characterised by the inflammation of gingiva and the progressive destruction of alveolar bone. The interaction between plaque microbes and host defence affects the process of the disease. As a new interdisciplinary field, osteoimmunology mainly studies the molecular interaction mechanism between skeletal and immune systems, which are related to the occurrence of periodontitis. MicroRNA 155 (miR-155) is an endogenous noncoding single-stranded RNA in eukaryotic organisms. miR-155 combines with the 3’-untranslated region of target mRNA to negatively regulate the expression of mRNA. miR-155 can participate in multiple physiological and pathological processes, such as immunity, haematopoiesis and inflammation. A large number of studies have shown that the expression level of miR-155 can be altered during periodontitis development, but results reported in literature are inconsistent. miR-155 can also regulate the skeletal system through multiple pathways. This review elaborates the modulation of miR-155 in osteoimmunology and periodontitis. We aim to offer novel insights and strategies for clinical therapy of periodontitis.

Key words: MicroRNA, osteoimmunology, periodontitis, bone metabolism, osteoblast, osteoclast

中图分类号: 

  • R781.4+2
[1] Papapanou PN, Sanz M, Buduneli N, et al. Perio-dontitis: consensus report of workgroup 2 of the 2017 World Workshop on the classification of perio-dontal and peri-implant diseases and conditions[J]. J Periodontol, 2018,89(Suppl 1):S173-S182.
doi: 10.1002/JPER.17-0721
[2] Soyocak A, Kurt H, Ozgen M, et al. miRNA-146a, miRNA-155 and JNK expression levels in peripheral blood mononuclear cells according to grade of knee osteoarthritis[J]. Gene, 2017,627:207-211.
doi: 10.1016/j.gene.2017.06.027 pmid: 28647559
[3] De Palma A, Cheleschi S, Pascarelli NA, et al. Hy-drostatic pressure as epigenetic modulator in chon-drocyte cultures: a study on miRNA-155, miRNA-181a and miRNA-223 expression levels[J]. J Biomech, 2018,66:165-169.
doi: 10.1016/j.jbiomech.2017.10.044 pmid: 29150345
[4] Radović N, Nikolić Jakoba N, Petrović N, et al. MicroRNA-146a and microRNA-155 as novel cre-vicular fluid biomarkers for periodontitis in non-dia-betic and type 2 diabetic patients[J]. J Clin Periodontol, 2018,45(6):663-671.
doi: 10.1111/jcpe.2018.45.issue-6
[5] Mashima R. Physiological roles of miR-155[J]. Im-munology, 2015,145(3):323-333.
[6] 李聪聪, 赵金艳, 吴姣, 等. miR-155研究进展[J]. 生物技术通报, 2018,34(11):70-82.
Li CC, Zhao JY, Wu J , et al. Research progress on miR-155[J]. Biotechnol Bull, 2018,34(11):70-82.
[7] Gebert LFR, MacRae IJ. Regulation of microRNA function in animals[J]. Nat Rev Mol Cell Biol, 2019,20(1):21-37.
doi: 10.1038/s41580-018-0045-7 pmid: 30108335
[8] Li N, Cui T, Guo W, et al. MiR-155-5p accelerates the metastasis of cervical cancer cell via targeting TP53INP1[J]. Onco Targets Ther, 2019,12:3181-3196.
doi: 10.2147/OTT.S193097 pmid: 31118671
[9] Liu F, Kong X, Lv L, et al. TGF-β1 acts through miR-155 to down-regulate TP53INP1 in promoting epithelial-mesenchymal transition and cancer stem cell phenotypes[J]. Cancer Lett, 2015,359(2):288-298.
doi: 10.1016/j.canlet.2015.01.030 pmid: 25633840
[10] Liu F, Kong X, Lv L, et al. MiR-155 targets TP53INP1 to regulate liver cancer stem cell acquisition and self-renewal[J]. FEBS Lett, 2015,589(4):500-506.
doi: 10.1016/j.febslet.2015.01.009 pmid: 25601564
[11] Nishimoto M, Nishikawa S, Kondo N, et al. Progno-stic impact of TP53INP1 gene expression in estrogen receptor α-positive breast cancer patients[J]. Jpn J Clin Oncol, 2019,49(6):567-575.
doi: 10.1093/jjco/hyz029 pmid: 30855679
[12] Costinean S, Zanesi N, Pekarsky Y, et al. Pre-B cell proliferation and lymphoblastic leukemia/high-grade lymphoma in Eμ-miR155 transgenic mice[J]. Proc Natl Acad Sci USA, 2006,103(18):7024-7029.
doi: 10.1073/pnas.0602266103 pmid: 16641092
[13] Wang C, Zhang C, Liu L, et al. Macrophage-derived mir-155-containing exosomes suppress fibroblast pro-liferation and promote fibroblast inflammation during cardiac injury[J]. Mol Ther, 2017,25(1):192-204.
doi: 10.1016/j.ymthe.2016.09.001 pmid: 28129114
[14] Stanczyk J, Pedrioli DM, Brentano F, et al. Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis[J]. Arthritis Rheum, 2008,58(4):1001-1009.
doi: 10.1002/art.23386 pmid: 18383392
[15] Churov AV, Oleinik EK, Knip M. MicroRNAs in rheumatoid arthritis: altered expression and diagno-stic potential[J]. Autoimmun Rev, 2015,14(11):1029-1037.
doi: 10.1016/j.autrev.2015.07.005 pmid: 26164649
[16] Xie YF, Shu R, Jiang SY, et al. Comparison of micro- RNA profiles of human periodontal diseased and healthy gingival tissues[J]. Int J Oral Sci, 2011,3(3):125-134.
doi: 10.4248/IJOS11046 pmid: 21789961
[17] Algate K, Haynes DR, Bartold PM, et al. The effects of tumour necrosis factor-α on bone cells involved in periodontal alveolar bone loss; osteoclasts, osteoblasts and osteocytes[J]. J Periodontal Res, 2016,51(5):549-566.
doi: 10.1111/jre.12339 pmid: 26667183
[18] Charles JF, Aliprantis AO. Osteoclasts: more than ‘bone eaters’[J]. Trends Mol Med, 2014,20(8):449-459.
doi: 10.1016/j.molmed.2014.06.001 pmid: 25008556
[19] Baum R, Gravallese EM. Bone as a target organ in rheumatic disease: impact on osteoclasts and osteo-blasts[J]. Clin Rev Allergy Immunol, 2016,51(1):1-15.
doi: 10.1007/s12016-015-8515-6 pmid: 26411424
[20] Arron JR, Choi Y. Bone versus immune system[J]. Nature, 2000,408(6812):535-536.
doi: 10.1038/35046196 pmid: 11117729
[21] Tang M, Tian L, Luo G, et al. Interferon-gamma-mediated osteoimmunology[J]. Front Immunol, 2018,9:1508.
doi: 10.3389/fimmu.2018.01508 pmid: 30008722
[22] Sato K, Suematsu A, Okamoto K, et al. Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction[J]. J Exp Med, 2006,203(12):2673-2682.
pmid: 17088434
[23] Kim YG, Park JW, Lee JM, et al. IL-17 inhibits oste-oblast differentiation and bone regeneration in rat[J]. Arch Oral Biol, 2014,59(9):897-905.
doi: 10.1016/j.archoralbio.2014.05.009 pmid: 24907519
[24] 谭静怡. 不同表型Th17细胞的诱导分化及其特征性分泌因子(IL-17/IFN-γ)在大鼠实验性牙周炎模型中的作用和相关机制研究[D]. 杭州: 浙江大学, 2018.
Tang JY . Study on different Th17 cell phenotypes differentiation and the effects of their characteristic secretory cytokines (IL-17/IFN-γ) in rats experimental periodontitis model and the associated mechanisms[D]. Hangzhou: Zhejiang University, 2018.
[25] Wang Z, Tan J, Lei L, et al. The positive effects of secreting cytokines IL-17 and IFN-γ on the early-stage differentiation and negative effects on the cal-cification of primary osteoblasts in vitro[J]. Int Im-munopharmacol, 2018,57:1-10.
[26] Bozec A, Zaiss MM, Kagwiria R, et al. T cell cos-timulation molecules CD80/86 inhibit osteoclast differentiation by inducing the IDO/tryptophan path-way[J]. Sci Transl Med, 2014, 6(235): 235ra60.
doi: 10.1126/scitranslmed.3008487 pmid: 24807555
[27] Pacifici R. T cells, osteoblasts, and osteocytes: in-teracting lineages key for the bone anabolic and catabolic activities of parathyroid hormone[J]. Ann N Y Acad Sci, 2016,1364:11-24.
doi: 10.1111/nyas.12969 pmid: 26662934
[28] Luo CY, Wang L, Sun C, et al. Estrogen enhances the functions of CD4+CD25+Foxp3+ regulatory T cells that suppress osteoclast differentiation and bone re-sorption in vitro [J]. Cell Mol Immunol, 2011,8(1):50-58.
doi: 10.1038/cmi.2010.54 pmid: 21200384
[29] Takayanagi H, Ogasawara K, Hida S, et al. T-cell-mediated regulation of osteoclastogenesis by signal-ling cross-talk between RANKL and IFN-γ[J]. Nature, 2000,408(6812):600-605.
doi: 10.1038/35046102 pmid: 11117749
[30] Takayanagi H. Osteoimmunology and the effects of the immune system on bone[J]. Nat Rev Rheumatol, 2009,5(12):667-676.
doi: 10.1038/nrrheum.2009.217 pmid: 19884898
[31] 陈之光, 薛今琦, 付勤. 干扰素-γ在骨免疫系统中作用的研究进展[J]. 中国骨质疏松杂志, 2015,21(3):361-366.
Chen ZG, Xue LQ, Fu Q . Research progress in the role of IFN-γ in osteoimmunology[J]. Chin J Osteopor, 2015,21(3):361-366.
[32] Weitzmann MN. Bone and the immune system[J]. Toxicol Pathol, 2017,45(7):911-924.
pmid: 29046115
[33] Li Y, Toraldo G, Li A, et al. B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo[J]. Blood, 2007,109(9):3839-3848.
doi: 10.1182/blood-2006-07-037994 pmid: 17202317
[34] Onal M, Xiong J, Chen X, et al. Receptor activator of nuclear factor κB ligand (RANKL) protein expre-ssion by B lymphocytes contributes to ovariectomy-induced bone loss[J]. J Biol Chem, 2012,287(35):29851-29860.
doi: 10.1074/jbc.M112.377945 pmid: 22782898
[35] Rivollier A, Mazzorana M, Tebib J, et al. Immature dendritic cell transdifferentiation into osteoclasts: a novel pathway sustained by the rheumatoid arthritis microenvironment[J]. Blood, 2004,104(13):4029-4037.
doi: 10.1182/blood-2004-01-0041 pmid: 15308576
[36] Horwood NJ. Macrophage polarization and bone formation: a review[J]. Clin Rev Allergy Immunol, 2016,51(1):79-86.
pmid: 26498771
[37] 罗亚东. Aire通过miR-155调控M1型巨噬细胞极化的研究[D]. 长春: 吉林大学, 2018.
Luo YD . Aire regulates the polarization of M1 ma-crophages through miR-155[D]. Changchun: Jilin University, 2018.
[38] He D, Kou X, Luo Q, et al. Enhanced M1/M2 ma-crophage ratio promotes orthodontic root resorption[J]. J Dent Res, 2015,94(1):129-139.
doi: 10.1177/0022034514553817 pmid: 25344334
[39] Zhang Q, Atsuta I, Liu S, et al. IL-17-mediated M1/M2 macrophage alteration contributes to pathoge-nesis of bisphosphonate-related osteonecrosis of the jaws[J]. Clin Cancer Res, 2013,19(12):3176-3188.
doi: 10.1158/1078-0432.CCR-13-0042 pmid: 23616636
[40] Wu X, Xu W, Feng X, et al. TNF-a mediated in-flammatory macrophage polarization contributes to the pathogenesis of steroid-induced osteonecrosis in mice[J]. Int J Immunopathol Pharmacol, 2015,28(3):351-361.
pmid: 26197804
[41] Hajishengallis G, Moutsopoulos NM, Hajishengallis E, et al. Immune and regulatory functions of neutro-phils in inflammatory bone loss[J]. Semin Immunol, 2016,28(2):146-158.
doi: 10.1016/j.smim.2016.02.002 pmid: 26936034
[42] Söderström K, Stein E, Colmenero P, et al. Natural killer cells trigger osteoclastogenesis and bone des-truction in arthritis[J]. Proc Natl Acad Sci USA, 2010,107(29):13028-13033.
doi: 10.1073/pnas.1000546107 pmid: 20615964
[43] Terashima A, Okamoto K, Nakashima T, et al. Sepsis-induced osteoblast ablation causes immunodeficiency[J]. Immunity, 2016,44(6):1434-1443.
doi: 10.1016/j.immuni.2016.05.012 pmid: 27317262
[44] Yu VW, Saez B, Cook C, et al. Specific bone cells produce DLL4 to generate thymus-seeding pro-genitors from bone marrow[J]. J Exp Med, 2015,212(5):759-774.
doi: 10.1084/jem.20141843 pmid: 25918341
[45] Greenbaum A, Hsu YM, Day RB, et al. CXCL12 in early mesenchymal progenitors is required for hae-matopoietic stem-cell maintenance[J]. Nature, 2013,495(7440):227-230.
doi: 10.1038/nature11926 pmid: 23434756
[46] Rankin EB, Wu C, Khatri R, et al. The HIF signaling pathway in osteoblasts directly modulates erythro-poiesis through the production of EPO[J]. Cell, 2012,149(1):63-74.
doi: 10.1016/j.cell.2012.01.051 pmid: 22464323
[47] Visnjic D, Kalajzic I, Gronowicz G, et al. Condi-tional ablation of the osteoblast lineage in Col2.3de-ltatk transgenic mice[J]. J Bone Miner Res, 2001,16(12):2222-2231.
doi: 10.1359/jbmr.2001.16.12.2222 pmid: 11760835
[48] Visnjic D, Kalajzic Z, Rowe DW, et al. Hemato-poiesis is severely altered in mice with an induced osteoblast deficiency[J]. Blood, 2004,103(9):3258-3264.
doi: 10.1182/blood-2003-11-4011 pmid: 14726388
[49] Yamazaki S, Ema H, Karlsson G, et al. Nonmyelina-ting Schwann cells maintain hematopoietic stem cell hibernation in the bone marrow niche[J]. Cell, 2011,147(5):1146-1158.
doi: 10.1016/j.cell.2011.09.053 pmid: 22118468
[50] Adams GB, Chabner KT, Alley IR, et al. Stem cell engraftment at the endosteal niche is specified by the calcium-sensing receptor[J]. Nature, 2006,439(7076):599-603.
pmid: 16382241
[51] Lymperi S, Ersek A, Ferraro F, et al. Inhibition of osteoclast function reduces hematopoietic stem cell numbers in vivo[J]. Blood, 2011,117(5):1540-1549.
pmid: 21131587
[52] Cain CJ, Rueda R, McLelland B, et al. Absence of sclerostin adversely affects B-cell survival[J]. J Bone Miner Res, 2012,27(7):1451-1461.
doi: 10.1002/jbmr.1608 pmid: 22434688
[53] Fulzele K, Krause DS, Panaroni C, et al. Myelo-poiesis is regulated by osteocytes through Gsαdepen-dent signaling[J]. Blood, 2013,121(6):930-939.
[54] 孟焕新. 牙周病学[M]. 4版. 北京: 人民卫生出版社, 2016: 96-98.
Meng HX. Periodontology[M]. 4th ed. Beijing: People’s Medical Publishing House, 2016: 96-98.
[55] Tao Y, Ai R, Hao Y, et al. Role of miR-155 in immune regulation and its relevance in oral lichen planus[J]. Exp Ther Med, 2019,17(1):575-586.
doi: 10.3892/etm.2018.7019 pmid: 30651838
[56] Rodriguez A, Vigorito E, Clare S, et al. Requirement of bic/microRNA-155 for normal immune function[J]. Science, 2007,316(5824):608-611.
doi: 10.1126/science.1139253 pmid: 17463290
[57] Thai TH, Calado DP, Casola S, et al. Regulation of the germinal center response by microRNA-155[J]. Science, 2007,316(5824):604-608.
doi: 10.1126/science.1141229 pmid: 17463289
[58] Zhang X, Hua F, Yang Z, et al. Enhancement of im-munoregulatory function of modified bone marrow mesenchymal stem cells by targeting SOCS1[J]. Bio-med Res Int, 2018,2018:3530647.
[59] Fan F, Shi P, Liu M, et al. Lactoferrin preserves bone homeostasis by regulating the RANKL/RANK/OPG pathway of osteoimmunology[J]. Food Funct, 2018,9(5):2653-2660.
[60] Ujiie Y, Karakida T, Yamakoshi Y, et al. Interleukin-4 released from human gingival fibroblasts reduces osteoclastogenesis[J]. Arch Oral Biol, 2016,72:187-193.
doi: 10.1016/j.archoralbio.2016.08.024 pmid: 27608363
[61] Zhang L, Ding Y, Rao GZ, et al. Effects of IL-10 and glucose on expression of OPG and RANKL in human periodontal ligament fibroblasts[J]. Braz J Med Biol Res, 2016,49(4):e4324.
doi: 10.1590/1414-431X20154324 pmid: 27074164
[62] Yao R, Ma YL, Liang W, et al. MicroRNA-155 mo-dulates Treg and Th17 cells differentiation and Th17 cell function by targeting SOCS1[J]. PLoS One, 2012,7(10):e46082.
doi: 10.1371/journal.pone.0046082 pmid: 23091595
[63] Dunand-Sauthier I, Irla M, Carnesecchi S, et al. Re-pression of arginase-2 expression in dendritic cells by microRNA-155 is critical for promoting T cell proliferation[J]. J Immunol, 2014,193(4):1690-1700.
doi: 10.4049/jimmunol.1301913 pmid: 25009204
[64] Martinez-Nunez RT, Louafi F, Sanchez-Elsner T. The interleukin 13 (IL-13) pathway in human macro-phages is modulated by microRNA-155 via direct targeting of interleukin 13 receptor α1 (IL13Rα1)[J]. J Biol Chem, 2011,286(3):1786-1794.
doi: 10.1074/jbc.M110.169367 pmid: 21097505
[65] Zhang Y, Mei H, Chang X, et al. Adipocyte-derived microvesicles from obese mice induce M1 macro-phage phenotype through secreted miR-155[J]. J Mol Cell Biol, 2016,8(6):505-517.
doi: 10.1093/jmcb/mjw040 pmid: 27671445
[66] Li B. MicroRNA regulation in osteogenic and adi-pogenic differentiation of bone mesenchymal stem cells and its application in bone regeneration[J]. Curr Stem Cell Res Ther, 2018,13(1):26-30.
doi: 10.2174/1574888X12666170605112727 pmid: 28578644
[67] Hou Q, Huang Y, Liu Y, et al. Profiling the miRNA-mRNA-lncRNA interaction network in MSC osteo-blast differentiation induced by (+)-cholesten-3-one[J]. BMC Genomics, 2018,19(1):783.
pmid: 30373531
[68] Gu Y, Ma L, Song L, et al. miR-155 inhibits mouse osteoblast differentiation by suppressing SMAD5 expression[J]. Biomed Res Int, 2017,2017:1893520.
pmid: 28473977
[69] Liu H, Zhong L, Yuan T, et al. MicroRNA-155 inhibits the osteogenic differentiation of mesenchymal stem cells induced by BMP9 via downregulation of BMP signaling pathway[J]. Int J Mol Med, 2018,41(6):3379-3393.
doi: 10.3892/ijmm.2018.3526 pmid: 29512689
[70] Asagiri M, Takayanagi H. The molecular understan-ding of osteoclast differentiation[J]. Bone, 2007,40(2):251-264.
doi: 10.1016/j.bone.2006.09.023 pmid: 17098490
[71] Hienz SA, Paliwal S, Ivanovski S. Mechanisms of bone resorption in periodontitis[J]. J Immunol Res, 2015,2015:615486.
doi: 10.1155/2015/615486 pmid: 26065002
[72] Sul OJ, Sung YB, Rajasekaran M, et al. MicroRNA- 155 induces autophagy in osteoclasts by targeting transforming growth factor β-activated kinase 1- binding protein 2 upon lipopolysaccharide stimulation[J]. Bone, 2018,116:279-289.
doi: 10.1016/j.bone.2018.08.014 pmid: 30144578
[73] Zhao H, Zhang J, Shao H, et al. Transforming growth factor β1/Smad4 signaling affects osteoclast dif-ferentiation via regulation of miR-155 expression[J]. Mol Cells, 2017,40(3):211-221.
doi: 10.14348/molcells.2017.2303 pmid: 28359146
[74] Zhang J, Zhao H, Chen J, et al. Interferon-β-induced miR-155 inhibits osteoclast differentiation by targe-ting SOCS1 and MITF[J]. FEBS Lett, 2012,586(19):3255-3262.
doi: 10.1016/j.febslet.2012.06.047
[75] Jing W, Zhang X, Sun W, et al. CRISPR/CAS9-mediated genome editing of miRNA-155 inhibits proinflammatory cytokine production by RAW264.7 cells[J]. Biomed Res Int, 2015,2015:326042.
doi: 10.1155/2015/326042 pmid: 26697483
[76] Hajishengallis G, Darveau RP, Curtis MA. The key-stone-pathogen hypojournal[J]. Nat Rev Microbiol, 2012,10(10):717-725.
doi: 10.1038/nrmicro2873 pmid: 22941505
[77] Xie Y, Sun M, Xia Y, et al. An RNA-seq screen of P. gingivalis LPS treated human gingival fibroblasts[J]. Arch Oral Biol, 2018,88:77-84.
doi: 10.1016/j.archoralbio.2018.01.002 pmid: 29407755
[78] Nayar G, Gauna A, Chukkapalli S, et al. Polymicro-bial infection alter inflammatory microRNA in rat salivary glands during periodontal disease[J]. Anae-robe, 2016,38:70-75.
[79] Stoecklin-Wasmer C, Guarnieri P, Celenti R, et al. MicroRNAs and their target genes in gingival tissues[J]. J Dent Res, 2012,91(10):934-940.
doi: 10.1177/0022034512456551 pmid: 22879578
[80] Chen SC, Constantinides C, Kebschull M, et al. MicroRNAs regulate cytokine responses in gingival epithelial cells[J]. Infect Immun, 2016,84(12):3282-3289.
doi: 10.1128/IAI.00263-16 pmid: 27600506
[81] Zheng Y, Dong C, Yang J, et al. Exosomal microRNA-155-5p from PDLSCs regulated Th17/Treg balance by targeting sirtuin-1 in chronic periodontitis[J]. J Cell Physiol, 2019,234(11):20662-20674.
pmid: 31016751
[82] Lim HW, Kang SG, Ryu JK, et al. SIRT1 deacety-lates RORγt and enhances Th17 cell generation[J]. J Exp Med, 2015,212(5):607-617.
doi: 10.1084/jem.20132378 pmid: 25918343
[83] Garlet GP, Cardoso CR, Campanelli AP, et al. Ex-pression of suppressors of cytokine signaling in dis-eased periodontal tissues: a stop signal for disease progression[J]. J Periodontal Res, 2006,41(6):580-584.
doi: 10.1111/j.1600-0765.2006.00908.x pmid: 17076785
[1] 傅豫, 何薇, 黄兰. 铁死亡在口腔疾病中的研究进展[J]. 国际口腔医学杂志, 2024, 51(1): 36-44.
[2] 周金阔,张晋弘,史晓晶,刘广顺,姜磊,刘倩峰. 长链非编码RNA小核仁RNA宿主基因22调控微小RNA-27b-3p对口腔鳞状细胞癌细胞增殖、侵袭和迁移的影响[J]. 国际口腔医学杂志, 2024, 51(1): 52-59.
[3] 李立恒,王蕊,王晓明,张智轶,张璇,安峰,王芹,张凡. 环状RNA hsa_circ_0085576调控微小RNA-498/B细胞特异性莫洛尼鼠白血病病毒整合位点1轴对口腔鳞状细胞癌细胞迁移和侵袭的影响[J]. 国际口腔医学杂志, 2024, 51(1): 60-67.
[4] 罗晓洁,王德续,陈晓涛. 基于生物信息学分析铁死亡调控基因与牙周炎的关系[J]. 国际口腔医学杂志, 2023, 50(6): 661-668.
[5] 黄元鸿,彭显,周学东. 骨碎补在治疗口腔骨相关疾病的研究进展[J]. 国际口腔医学杂志, 2023, 50(6): 679-685.
[6] 余岳霖,孔卫东. 甲状旁腺激素受体1基因相关与原发性牙齿萌出障碍的研究进展[J]. 国际口腔医学杂志, 2023, 50(5): 573-580.
[7] 龚美灵,程兴群,吴红崑. 牙周炎与帕金森病相关性的研究进展[J]. 国际口腔医学杂志, 2023, 50(5): 587-593.
[8] 孙佳,韩烨,侯建霞. 白细胞介素-6-铁调素信号轴调控牙周炎相关性贫血致病机制的研究进展[J]. 国际口腔医学杂志, 2023, 50(3): 329-334.
[9] 刘体倩,梁星,刘蔚晴,李晓虹,朱睿. 咬合创伤在牙周炎发生发展中的作用及机制的研究进展[J]. 国际口腔医学杂志, 2023, 50(1): 19-24.
[10] 李琼,于维先. 白藜芦醇治疗牙周炎及其生物利用度的研究进展[J]. 国际口腔医学杂志, 2023, 50(1): 25-31.
[11] 黄伟琨,徐秋艳,周婷. 黄芩苷抑制脂多糖促巨噬细胞氧化应激损伤作用的研究[J]. 国际口腔医学杂志, 2022, 49(5): 521-528.
[12] 周剑鹏,谢旭东,赵蕾,王骏. 辅助性T细胞17及白细胞介素17在牙周炎中的作用及机制的研究进展[J]. 国际口腔医学杂志, 2022, 49(5): 586-592.
[13] 陈荟宇,白明茹,叶玲. 信号素3A与口腔常见病关系的研究进展[J]. 国际口腔医学杂志, 2022, 49(5): 593-599.
[14] 张静怡,李丹薇,孙宇,雷雅燕,刘涛,龚瑜. 复合树脂及复合体对成骨细胞毒性及成骨向分化的影响[J]. 国际口腔医学杂志, 2022, 49(4): 412-419.
[15] 周佳佳,赵蕾,徐欣. 牙周炎相关基因多态性的研究进展[J]. 国际口腔医学杂志, 2022, 49(4): 432-440.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
[1] 张新春. 桩冠修复与无髓牙的保护[J]. 国际口腔医学杂志, 1999, 26(06): .
[2] 王昆润. 长期单侧鼻呼吸对头颅发育有不利影响[J]. 国际口腔医学杂志, 1999, 26(05): .
[3] 彭国光. 颈淋巴清扫术中颈交感神经干的解剖变异[J]. 国际口腔医学杂志, 1999, 26(05): .
[4] 杨凯. 淋巴化疗的药物运载系统及其应用现状[J]. 国际口腔医学杂志, 1999, 26(05): .
[5] 康非吾. 种植义齿下部结构生物力学研究进展[J]. 国际口腔医学杂志, 1999, 26(05): .
[6] 柴枫. 可摘局部义齿用Co-Cr合金的激光焊接[J]. 国际口腔医学杂志, 1999, 26(04): .
[7] 孟姝,吴亚菲,杨禾. 伴放线放线杆菌产生的细胞致死膨胀毒素及其与牙周病的关系[J]. 国际口腔医学杂志, 2005, 32(06): 458 -460 .
[8] 费晓露,丁一,徐屹. 牙周可疑致病菌对口腔黏膜上皮的粘附和侵入[J]. 国际口腔医学杂志, 2005, 32(06): 452 -454 .
[9] 赵兴福,黄晓晶. 变形链球菌蛋白组学研究进展[J]. 国际口腔医学杂志, 2008, 35(S1): .
[10] 庞莉苹,姚江武. 抛光和上釉对陶瓷表面粗糙度、挠曲强度及磨损性能的影响[J]. 国际口腔医学杂志, 2008, 35(S1): .