国际口腔医学杂志

国际口腔医学杂志 ›› 2020, Vol. 47 ›› Issue (1): 76-83.doi: 10.7518/gjkq.2020004

• 综述 • 上一篇    下一篇

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

周婕妤,刘琳,吴亚菲,赵蕾()   

  1. 口腔疾病研究国家重点实验室 国家口腔疾病临床医学研究中心 四川大学华西口腔医院牙周病科 成都 610041
  • 收稿日期:2019-05-08 修回日期:2019-09-12 出版日期:2020-01-01 发布日期:2020-01-01
  • 作者简介:周婕妤,博士,Email： 453499723@qq.com
  • 基金资助:
    国家自然科学基金(81771077);国家自然科学基金(81970944);四川省科学技术厅基金(2018SZ01161)

Research progress on microRNA-mediated mechanisms between periodontitis and atherosclerosis

Zhou Jieyu,Liu Lin,Wu Yafei,Zhao Lei()   

  1. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Periodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2019-05-08 Revised:2019-09-12 Online:2020-01-01 Published:2020-01-01
  • Supported by:
    This study was supported by National Natural and Science Foundation of China(81771077);This study was supported by National Natural and Science Foundation of China(81970944);Fund of Science and Technology Department of Sichuan Province(2018SZ01161)

RichHTML

17

PDF (PC)

621

摘要：

牙周炎是一种主要由菌斑生物膜所引起的牙周支持组织慢性炎症破坏性疾病,与宿主的免疫反应相关。牙周致病菌可通过一过性菌血症进入血液循环系统,引发血管炎症反应,增加心血管疾病患病风险。微小RNA（microRNA）作为近年来小分子RNA的研究热点,可在表观遗传学水平调控基因表达,参与炎症调节。本文综述了牙周致病菌通过microRNA调控免疫炎症反应的机制,从而介导动脉粥样硬化的发生、发展,为牙周炎与动脉粥样硬化疾病关联的分子机制研究提供新的思路。此外,通过探索动脉粥样硬化与牙周炎相关特异性microRNA的表达模式,可为未来诊断或治疗心血管疾病提供新的参考。

关键词: 牙周致病菌, 牙周炎, 动脉粥样硬化, 心血管疾病, 微小RNA

Abstract:

Periodontitis is a chronic inflammatory disease characterised by destruction of periodontal supporting tissue, which is mainly due to plaque biofilm and host immune response. Periodontal pathogen can invade the blood circulation system by transient bacteraemia and trigger the vascular inflammation, which can definitely increase the risk of cardiovascular disease. MicroRNA, a small molecule RNA discussed in this paper, can regulate gene expression in epigenetics and participate in the regulation of inflammation. This review focuses on the mechanism of how periodontal pathogens regulate immune inflammatory response by microRNA to mediate the generation and development of atherosclerosis, which can provide new ideas for the research on the linkages on molecular mechanism between periodontitis and atherosclerosis. Moreover, exploring the specific microRNA expression patterns related to atherosclerosis and periodontitis can serve as a theoretical basis for the diagnosis and treatment of cardiovascular diseases in the future.

Key words: periodontal pathogen, periodontitis, atherosclerosis, cardiovascular disease, microRNA

中图分类号: 

  • R781.4 +2
[1] Gibson FC 3rd, Yumoto H, Takahashi Y , et al. Innate immune signaling and Porphyromonas gingivalis-accelerated atherosclerosis[J]. J Dent Res, 2006,85(2):106-121.
[2] Fabian MR, Sonenberg N, Filipowicz W . Regulation of mRNA translation and stability by microRNAs[J]. Annu Rev Biochem, 2010,79:351-379.
[3] Nahid MA, Pauley KM, Satoh M , et al. miR-146a is critical for endotoxin-induced tolerance: implication in innate immunity[J]. J Biol Chem, 2009,284(50):34590-34599.
[4] Alam MM ,O’Neill LA . MicroRNAs and the resolution phase of inflammation in macrophages[J]. Eur J Im-munol, 2011,41(9):2482-2485.
[5] Caescu CI, Guo X, Tesfa L , et al. Colony stimulating factor-1 receptor signaling networks inhibit mouse macrophage inflammatory responses by induction of microRNA-21[J]. Blood, 2015,125(8):e1-e13.
[6] Cheng Y, Du L, Jiao H , et al. Mmu-miR-27a-5p-dependent upregulation of MCPIP1 inhibits the in-flammatory response in LPS-induced RAW264.7 macrophage cells[J]. Biomed Res Int, 2015,2015:607692.
[7] Lai L, Song Y, Liu Y , et al. MicroRNA-92a nega-tively regulates Toll-like receptor (TLR)-triggered inflammatory response in macrophages by targeting MKK4 kinase[J]. J Biol Chem, 2013,288(11):7956-7967.
[8] Sun Y, Qin Z, Li Q , et al. MicroRNA-124 negatively regulates LPS-induced TNF-α production in mouse macrophages by decreasing protein stability[J]. Acta Pharmacol Sin, 2016,37(7):889-897.
[9] Fan G, Jiang X, Wu X , et al. Anti-inflammatory ac-tivity of tanshinone IIA in LPS-stimulated RAW264.7 macrophages via miRNAs and TLR4-NF-κB path-way[J]. Inflammation, 2016,39(1):375-384.
[10] Huang L, Ma Q, Li Y , et al. Inhibition of microRNA- 210 suppresses pro-inflammatory response and re-duces acute brain injury of ischemic stroke in mice[J]. Exp Neurol, 2018,300:41-50.
[11] Luan X, Zhou X, Trombetta-eSilva J, , et al. MicroRNAs and periodontal homeostasis[J]. J Dent Res, 2017,96(5):491-500.
[12] Lee YH, Na HS, Jeong SY , et al. Comparison of in-flammatory microRNA expression in healthy and periodontitis tissues[J]. Biocell, 2011,35(2):43-49.
[13] Xie YF, Shu R, Jiang SY , et al. Comparison of microRNA profiles of human periodontal diseased and healthy gingival tissues[J]. Int J Oral Sci, 2011,3(3):125-134.
[14] 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.
[15] Ogata Y, Matsui S, Kato A , et al. MicroRNA expre-ssion in inflamed and noninflamed gingival tissues from Japanese patients[J]. J Oral Sci, 2014,56(4):253-260.
[16] Venugopal P, Koshy T, Lavu V , et al. Differential expression of microRNAs let-7a, miR-125b, miR- 100, and miR-21 and interaction with NF-κB pathway genes in periodontitis pathogenesis[J]. J Cell Physiol, 2018,233(8):5877-5884.
[17] Amaral SA, Pereira TSF, Brito JAR , et al. Comparison of miRNA expression profiles in individuals with chronic or aggressive periodontitis[J]. Oral Dis, 2019,25(2):561-568.
[18] Motedayyen H, Ghotloo S, Saffari M , et al. Evalua-tion of microRNA-146a and its targets in gingival tissues of patients with chronic periodontitis[J]. J Periodontol, 2015,86(12):1380-1385.
[19] Radović N, Nikolić Jakoba N, Petrović N , et al. MicroRNA-146a and microRNA-155 as novel cre-vicular fluid biomarkers for periodontitis in nondia-betic and type 2 diabetic patients[J]. J Clin Periodon- tol, 2018,45(6):663-671.
[20] Yoneda T, Tomofuji T, Ekuni D , et al. Serum micro-RNAs and chronic periodontitis: a case-control study[J]. Arch Oral Biol, 2019,101:57-63.
[21] Tomofuji T, Yoneda T, Machida T , et al. MicroRNAs as serum biomarkers for periodontitis[J]. J Clin Pe-riodontol, 2016,43(5):418-425.
[22] Bagavad Gita J, George AV, Pavithra N , et al. Dysre-gulation of miR-146a by periodontal pathogens: a risk for acute coronary syndrome[J]. J Periodontol, 2019,90(7):756-765.
[23] Guo M, Mao X, Ji Q , et al. miR-146a in PBMCs modulates Th1 function in patients with acute coronary syndrome[J]. Immunol Cell Biol, 2010,88(5):555-564.
[24] Nahid MA, Rivera M, Lucas A , et al. Polymicrobial infection with periodontal pathogens specifically enhances microRNA miR-146a in ApoE -/- mice during experimental periodontal disease [J]. Infect Immun, 2011,79(4):1597-1605.
[25] Xuan Y, Gao Y, Huang H , et al. Tanshinone IIA at-tenuates atherosclerosis in apolipoprotein E knockout mice infected with Porphyromonas gingivalis[J]. Inflammation, 2017,40(5):1631-1642.
[26] Jia R, Hashizume-Takizawa T, Du Y , et al. Aggregati-bacter actinomycetemcomitans induces Th17 cells in atherosclerotic lesions[J]. Pathog Dis, 2015,73(3). doi: 10.1093/femspd/ftu027.
[27] Hajishengallis G . Periodontitis: from microbial im-mune subversion to systemic inflammation[J]. Nat Rev Immunol, 2015,15(1):30-44.
[28] Urbich C, Kuehbacher A, Dimmeler S . Role of microRNAs in vascular diseases, inflammation, and angiogenesis[J]. Cardiovasc Res, 2008,79(4):581-588.
[29] Renzi TA, Rubino M, Gornati L , et al. MiR-146b mediates endotoxin tolerance in human phagocytes[J]. Mediators Inflamm, 2015,2015:145305.
[30] Li X, Ji Z, Li S , et al. miR-146a-5p antagonized AGEs- and P.g-LPS-induced ABCA1 and ABCG1 dysregulation in macrophages via IRAK-1 downre-gulation[J]. Inflammation, 2015,38(5):1761-1768.
[31] Molteni M, Bosi A, Saturni V , et al. MiR-146a in-duction by cyanobacterial lipopolysaccharide anta-gonist (CyP) mediates endotoxin cross-tolerance[J]. Sci Rep, 2018,8(1):11367.
[32] Molteni M, Bosi A, Rossetti C . The effect of cyano-bacterial LPS antagonist (CyP) on cytokines and micro-RNA expression induced by Porphyromonas gingivalis LPS[J]. Toxins (Basel), 2018,10(7). doi: 10.3390/toxins10070290.
[33] Honda T, Takahashi N, Miyauchi S , et al. Porphyro-monas gingivalis lipopolysaccharide induces miR-146a without altering the production of inflammatory cytokines[J]. Biochem Biophys Res Commun, 2012,420(4):918-925.
[34] Tsai PC, Liao YC, Wang YS , et al. Serum microRNA- 21 and microRNA-221 as potential biomarkers for cerebrovascular disease[J]. J Vasc Res, 2013,50(4):346-354.
[35] Canfrán-Duque A, Rotllan N, Zhang X , et al. Macro-phage deficiency of miR-21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis[J]. EMBO Mol Med, 2017,9(9):1244-1262.
[36] Ruan Q, Wang P, Wang T , et al. MicroRNA-21 re-gulates T-cell apoptosis by directly targeting the tumor suppressor gene Tipe2[J]. Cell Death Dis, 2014,5:e1095.
[37] Niu J, Shi Y, Tan G , et al. DNA damage induces NF-κB-dependent microRNA-21 up-regulation and promotes breast cancer cell invasion[J]. J Biol Chem, 2012,287(26):21783-21795.
[38] Shin VY, Jin H, Ng EK , et al. NF-κB targets miR-16 and miR-21 in gastric cancer: involvement of prosta-glandin E receptors[J]. Carcinogenesis, 2011,32(2):240-245.
[39] Das A, Ganesh K, Khanna S , et al. Engulfment of apoptotic cells by macrophages: a role of microRNA- 21 in the resolution of wound inflammation[J]. J Immunol, 2014,192(3):1120-1129.
[40] Ji R, Cheng Y, Yue J , et al. MicroRNA expression signature and antisense-mediated depletion reveal an essential role of microRNA in vascular neointimal lesion formation[J]. Circ Res, 2007,100(11):1579-1588.
[41] Perdiguero E, Sousa-Victor P, Ruiz-Bonilla V , et al. p38/MKP-1-regulated AKT coordinates macrophage transitions and resolution of inflammation during tissue repair[J]. J Cell Biol, 2011,195(2):307-322.
[42] Wu Z, Lu H, Sheng J , et al. Inductive microRNA-21 impairs anti-mycobacterial responses by targeting IL-12 and Bcl-2[J]. FEBS Lett, 2012,586(16):2459-2467.
[43] Xue X, Qiu Y, Yang HL . Immunoregulatory role of microRNA-21 in macrophages in response to Bacillus calmette-guerin infection involves modulation of the TLR4/MyD88 signaling pathway[J]. Cell Physiol Biochem, 2017,42(1):91-102.
[44] Zhou W, Su L, Duan X , et al. MicroRNA-21 down-regulates inflammation and inhibits periodontitis[J]. Mol Immunol, 2018,101:608-614.
[45] Yang X, Pan Y, Xu X , et al. Sialidase deficiency in Porphyromonas gingivalis increases IL-12 secretion in stimulated macrophages through regulation of CR3, lncRNA GAS5 and miR-21[J]. Front Cell Infect Mi-crobiol, 2018,8:100.
[46] Huck O, Al-Hashemi J, Poidevin L , et al. Identi-fication and characterization of microRNA differen-tially expressed in macrophages exposed to Por-phyromonas gingivalis infection[J]. Infect Immun, 2017,85(3). doi: 10.1128/IAI.00771-16.
[47] Na HS, Park MH, Song YR , et al. Elevated micro-RNA-128 in periodontitis mitigates tumor necrosis factor-α response via p38 signaling pathway in macrophages[J]. J Periodontol, 2016,87(9):e173-e182.
[48] Park MH, Park E, Kim HJ , et al. Porphyromonas gingivalis-induced miR-132 regulates TNFα expre-ssion in THP-1 derived macrophages[J]. Springer-Plus, 2016,5:761.
[49] Naqvi AR, Fordham JB, Khan A , et al. MicroRNAs responsive to Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis LPS modulate ex-pression of genes regulating innate immunity in human macrophages[J]. Innate Immun, 2014,20(5):540-551.
[50] Fordham JB, Naqvi AR, Nares S. miR-24 regulates macrophage polarization and plasticity[J]. J Clin Cell Immunol, 2015,6:(5)pii: 362.
[51] Pessi T, Viiri LE, Raitoharju E , et al. Interleukin-6 and microRNA profiles induced by oral bacteria in human atheroma derived and healthy smooth muscle cells[J]. Springerplus, 2015,4:206.
[52] Laffont B, Rayner KJ . MicroRNAs in the pathobio-logy and therapy of atherosclerosis[J]. Can J Cardiol, 2017,33(3):313-324.
[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] 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.
[7] 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.
[8] 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.
[9] 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.
[10] 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.
[11] 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.
[12] 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.
[13] 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.
[14] 洪娅娅,陈学鹏,姒蜜思. 非编码RNA调控牙囊干细胞成骨分化的研究进展[J]. 国际口腔医学杂志, 2022, 49(3): 263-271.
[15] 马玉,左玉,张鑫. 光动力疗法辅助治疗牙周炎治疗效果的Meta分析[J]. 国际口腔医学杂志, 2022, 49(3): 305-316.
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): .