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)

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] 童钰鑫,肖新莉,安莹,张佳喻,石旭妍,王旭,陈悦. 慢性牙周炎对c57小鼠认知能力的影响[J]. 国际口腔医学杂志, 2020, 47(5): 530-537.
[2] 付世锦,曾刊,李鑫,杨静,汪成林,叶玲. 骨保护素/核因子κB受体活化因子配体影响肺癌细胞下颌骨与股骨转移差异的初步研究[J]. 国际口腔医学杂志, 2020, 47(5): 538-546.
[3] 杨佩佩,杨羽晨,张强. 尼古丁对牙槽骨破骨细胞的作用及其机制的研究进展[J]. 国际口腔医学杂志, 2020, 47(5): 616-620.
[4] 马凯,李昊,赵红梅,王永亮,刘杰,柏娜. 低温氩氧等离子体处理的无机牛骨对MC3T3-E1细胞黏附、增殖及分化的影响[J]. 国际口腔医学杂志, 2020, 47(3): 278-285.
[5] 王晓宇,朱昭蓉,吴亚菲,赵蕾. 中性粒细胞细胞外陷阱网与牙周炎的相关性研究进展[J]. 国际口腔医学杂志, 2020, 47(3): 304-310.
[6] 陈斌,徐蓉蓉,张家鼎,闫福华. 重度牙周炎患牙的保存治疗[J]. 国际口腔医学杂志, 2020, 47(2): 125-130.
[7] 崔钰嘉,孙建勋,周学东. 黄连素的生物学功能及治疗口腔疾病研究的进展[J]. 国际口腔医学杂志, 2020, 47(1): 115-120.
[8] 周婕妤,刘琳,吴亚菲,赵蕾. 微小RNA介导的牙周炎与动脉粥样硬化相关机制的研究进展[J]. 国际口腔医学杂志, 2020, 47(1): 76-83.
[9] 朱俊瑾,周佳琦,伍颖颖. 哺乳动物雷帕霉素靶蛋白复合物1介导的自噬对骨代谢的调控[J]. 国际口腔医学杂志, 2020, 47(1): 84-89.
[10] 卢可心,张迪亚,吴燕岷. 蛋白酶激活受体在牙周组织细胞中相关作用的研究进展[J]. 国际口腔医学杂志, 2019, 46(6): 657-662.
[11] 张智颖,刘东娟,潘亚萍. 牙龈卟啉单胞菌外膜囊泡的研究进展[J]. 国际口腔医学杂志, 2019, 46(6): 670-674.
[12] 姜亦洋,刘怡. 甲基化对牙周炎发生与发展的影响及临床应用[J]. 国际口腔医学杂志, 2019, 46(5): 593-603.
[13] 张佳喻,罗宁,苗棣,应绚,陈悦. 意向性牙再植治疗重度牙周炎患牙的临床研究[J]. 国际口腔医学杂志, 2019, 46(4): 400-406.
[14] 张誉泓,戚孟春,董伟,孙红. CaMKi>Ⅱδ基因沉默对破骨细胞分化功能及c-fosi>/c-juni>/CREBi>基因的影响[J]. 国际口腔医学杂志, 2019, 46(4): 420-425.
[15] 原振英,管翠强,南欣荣. DNA甲基化与口腔疾病的研究进展[J]. 国际口腔医学杂志, 2019, 46(4): 437-441.
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] 逄键梁. 两例外胚层发育不良儿童骨内植入种植体后牙槽骨生长情况[J]. 国际口腔医学杂志, 1999, 26(05): .
[4] 王昆润. 后牙冠根斜形牙折的治疗[J]. 国际口腔医学杂志, 1999, 26(05): .
[5] 王昆润. 下颔骨成形术用网状钛板固定植骨块[J]. 国际口腔医学杂志, 1999, 26(04): .
[6] 杨美祥. 前牙厚度在预测上下颌牙量协调性中的作用[J]. 国际口腔医学杂志, 1999, 26(04): .
[7] 王金涛 刘美娟 孙宏晨 欧阳喈. 牙槽嵴牵张成骨[J]. 国际口腔医学杂志, 2004, 31(02): 146 -148 .
[8] 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 .
[9] 轩东英,张建波 金岩. 胚胎发育期TGF-β超家族成员与腭裂发生的关系[J]. 国际口腔医学杂志, 2004, 31(02): 132 -134 .
[10] 张婷,莫安春. 暂时冠桥修复材料的研究进展[J]. 国际口腔医学杂志, 2008, 35(S1): .