国际口腔医学杂志 ›› 2019, Vol. 46 ›› Issue (6): 657-662.doi: 10.7518/gjkq.2019077

• 综述 • 上一篇    下一篇

蛋白酶激活受体在牙周组织细胞中相关作用的研究进展

卢可心1,张迪亚2,吴燕岷1   

  1. 1. 浙江大学医学院附属第二医院口腔内科 杭州 310009
    2. 浙江大学医学院附属邵逸夫医院牙科中心 杭州 310016
  • 收稿日期:2019-03-06 修回日期:2019-07-14 出版日期:2019-11-01 发布日期:2019-11-14
  • 作者简介:卢可心,学士,Email: 540604120@qq.com
  • 基金资助:
    国家自然科学基金(81000447);浙江省科学技术厅公益研究计划(LGF18H140003);浙江省自然科学基金(LY17H140002)

Research progress of protease-activated receptors on different types of cells in periodontal tissue

Lu Kexin1,Zhang Diya2,Wu Yanmin1   

  1. 1. Dept. of Oral Medicine, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China
    2. Dental Department, The Affiliated Sir Run Shaw Hospital, Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310016, China
  • Received:2019-03-06 Revised:2019-07-14 Online:2019-11-01 Published:2019-11-14
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81000447);Science and Technology Department Public Welfare Research Plan of Zhejiang Province(LGF18H140003);Natural Science Foundation of Zhejiang Province(LY17H140002)

摘要:

蛋白酶激活受体是一种可被多种内源性和外源性蛋白酶激活,参与炎症反应且分布广泛的跨膜蛋白。国内外研究者主要阐述不同类型蛋白酶激活受体在牙周炎中的作用,尚未出现系统性分类陈述蛋白酶激活受体在牙周组织不同细胞中的作用。本文就蛋白酶激活受体分别在牙龈上皮细胞、牙龈成纤维细胞、成骨细胞、破骨细胞、免疫细胞等牙周组织不同细胞中的表达及与牙周炎相关作用等研究进展进行综述。

关键词: 蛋白酶激活受体, 牙龈上皮细胞, 牙龈成纤维细胞, 成骨细胞, 破骨细胞

Abstract: Protease-activated receptors (PARs), which are widely expressed transmembrane proteins, may induce inflammatory response once activated by a variety of endogenous and bacterial enzymes. Gingival epithelial cells, gingival fibroblasts, osteoblasts, osteoclasts, monocytes, macrophages and T lymphocytes exist in the periodontal tissue. In the development of periodontitis, the activated PARs of these cells are involved in the release of inflammatory factors and chemokines that cause gingival inflammation and alveolar bone destruction. Up-to-date data has shown the roles of PAR-1 and PAR-2 in periodontitis. However, the roles of PARs in hinge on different types of cells in the periodontal tissue have not been reviewed. Thus, the present review will focus on the current progress in the expression and functions of PARs.

Key words: protease-activated receptor, gingival epithelial cell, gingival fibroblast, osteoblast, osteoclast

中图分类号: 

  • Q26
[1] Thilagar S, Santhanakrishnan M, Rao S . Expression of protease-activated receptors 1 and 2 in individuals with healthy gingiva and chronic periodontitis[J]. J Indian Soc Periodontol, 2018,22(1):12-17.
[2] Castro ML, Franco GC, Branco-de-Almeida LS, et al. Downregulation of proteinase-activated receptor- 2, interleukin-17, and other proinflammatory genes by subantimicrobial doxycycline dose in a rat perio-dontitis model[J]. J Periodontol, 2016,87(2):203-210.
[3] Zhang D, Li S, Hu L , et al. Modulation of protease-activated receptor expression by Porphyromonas gingivalis in human gingival epithelial cells[J]. BMC Oral Health, 2015,15(1):128.
[4] Pereira AL, Holzhausen M, Franco GC , et al. Human β-defensin 2 and protease activated receptor-2 expression in patients with chronic periodontitis[J]. Arch Oral Biol, 2012,57(12):1609-1614.
[5] Rohani MG, Beyer RP, Hacker BM , et al. Modulation of expression of innate immunity markers CXCL5/ENA-78 and CCL20/MIP3alpha by protease-activated receptors (PARs) in human gingival epithelial cells[J]. Innate Immun, 2010,16(2):104-114.
[6] Maeno M, Lee C, Kim DM , et al. Function of platelet-induced epithelial attachment at titanium surfaces inhibits microbial colonization[J]. J Dent Res, 2017,96(6):633-639.
[7] da Silva HA, Euzebio Alves VT, Spolidório LC , et al. Expression of protease activated receptor-1 in chronic periodontitis[J]. J Periodontol, 2014,85(12):1763-1769.
[8] Tada H, Matsuyama T, Nishioka T , et al. Porphyromonas gingivalis gingipain-dependently enhances IL-33 production in human gingival epithelial cells[J]. PLoS One, 2016,11(4):e0152794.
[9] Son GY, Son A, Yang YM , et al. Airborne allergens induce protease activated receptor-2-mediated production of inflammatory cytokines in human gingival epithelium[J]. Arch Oral Biol, 2016,61:138-143.
[10] Naylor AJ, Filer A, Buckley CD . The role of stromal cells in the persistence of chronic inflammation[J]. Clin Exp Immunol, 2013,171(1):30-35.
[11] Palm E, Demirel I, Bengtsson T , et al. The role of toll-like and protease-activated receptors and associated intracellular signaling in Porphyromonas gingivalis-infected gingival fibroblasts[J]. APMIS, 2017,125(2):157-169.
[12] Fukushima H, Alves VT, Carvalho VF , et al. PAR-2 expression in the gingival crevicular fluid reflects chronic periodontitis severity[J]. Braz Oral Res, 2017,31:e16.
[13] 张迪亚, 胡玲静, 李盛来 , 等. 牙龈成纤维细胞表达蛋白酶激活受体的类型及作用研究[J]. 中华口腔医学杂志, 2014,49(1):21-26.
Zhang DY, Hu LJ, Li SL , et al. Expressions of protease-actevated receptors in human gingival fibroblasts and its functions in periodontitis[J]. Chin J Stomatol, 2014,49(1):21-26.
[14] Palm E, Demirel I, Bengtsson T , et al. The role of toll-like and protease-activated receptors in the expression of cytokines by gingival fibroblasts stimulated with the periodontal pathogen Porphyromonas gingivalis[J]. Cytokine, 2015,76(2):424-432.
[15] Uehara A, Muramoto K, Imamura T , et al. Arginine-specific gingipains from Porphyromonas gingivalis stimulate production of hepatocyte growth factor (scatter factor) through protease-activated receptors in human gingival fibroblasts in culture[J]. J Immunol, 2005,175(9):6076-6084.
[16] Yang WH, Deng YT, Hsieh YP , et al. Thrombin activates latent TGFβ1 via integrin αvβ1 in gingival fibroblasts[J]. J Dent Res, 2016,95(8):939-945.
[17] Shen K, Murphy CM, Chan B , et al. Activated protein C (APC) can increase bone anabolism via a protease-activated receptor (PAR)1/2 dependent mechanism[J]. J Orthop Res, 2014,32(12):1549-1556.
[18] Yoshida K, Akita N, Okamoto T , et al. Activated protein C suppresses osteoclast differentiation via endothelial protein C receptor, protease-activated receptor-1, sphingosine 1-phosphate receptor, and apolipoprotein E receptor 2[J]. Thromb Res, 2018,163:30-40.
[19] Tudpor K, van der Eerden BC, Jongwattanapisan P , et al. Thrombin receptor deficiency leads to a high bone mass phenotype by decreasing the RANKL/OPG ratio[J]. Bone, 2015,72:14-22.
[20] Maeda Y, Sekiguchi F, Yamanaka R , et al. Mechanisms for proteinase-activated receptor 1-triggered prostaglandin E2 generation in mouse osteoblastic MC3T3-E1 cells[J]. Biol Chem, 2015,396(2):153-162.
[21] Sato N, Ichikawa J, Wako M , et al. Thrombin induced by the extrinsic pathway and PAR-1 regulated inflammation at the site of fracture repair[J]. Bone, 2016,83:23-34.
[22] Francis N, Ayodele BA, O’Brien-Simpson NM, et al. Keratinocyte-specific ablation of protease-activated receptor 2 prevents gingival inflammation and bone loss in a mouse model of periodontal disease[J]. Cell Microbiol, 2018,20(11):e12891.
[23] Jackson MT, Moradi B, Zaki S , et al. Depletion of protease-activated receptor 2 but not protease-ac-tivated receptor 1 may confer protection against osteoarthritis in mice through extracartilaginous mechanisms[J]. Arthritis Rheumatol, 2014,66(12):3337-3348.
[24] Kanno Y, Ishisaki A, Kawashita E , et al. uPA attenua-ted LPS-induced inflammatory osteoclastogenesis through the plasmin/PAR-1/Ca 2+/CaMKK/AMPK axis [J]. Int J Biol Sci, 2016,12(1):63-71.
[25] Antoniak S, Tatsumi K, Bode M , et al. Protease-activated receptor 1 enhances polyI:C induction of the antiviral response in macrophages and mice[J]. J Innate Immun, 2017,9(2):181-192.
[26] Chionh YT, Ng GZ, Ong L , et al. Protease-activated receptor 1 suppresses Helicobacter pylori gastritis via the inhibition of macrophage cytokine secretion and interferon regulatory factor 5[J]. Mucosal Immunol, 2015,8(1):68-79.
[27] Yamaguchi R, Yamamoto T, Sakamoto A , et al. Mechanism of interleukin-13 production by granulocyte-macrophage colony-stimulating factor-dependent macrophages via protease-activated receptor-2[J]. Blood Cells Mol Dis, 2015,55(1):21-26.
[28] Gleeson EM, O’Donnell JS, Hams E, et al. Activated factor X signaling via protease-activated receptor 2 suppresses pro-inflammatory cytokine production from lipopolysaccharide-stimulated myeloid cells[J]. Haematologica, 2014,99(1):185-193.
[29] Shrestha Palikhe N, Nahirney D, Laratta C , et al. In- creased protease-activated receptor-2 (PAR-2) ex-pression on CD14 ++CD16 + peripheral blood monocytes of patients with severe asthma [J]. PLoS One, 2015,10(12):e0144500.
[30] Dekita M, Wu Z, Ni J , et al. Cathepsin S is involved in Th17 differentiation through the upregulation of IL-6 by activating PAR-2 after systemic exposure to lipopolysaccharide from Porphyromonas gingivalis[J]. Front Pharmacol, 2017,8:470.
[31] Du L, Long Y, Kim JJ , et al. Protease activated receptor-2 induces immune activation and visceral hypersensitivity in post-infectious irritable bowel syndrome mice[J]. Dig Dis Sci, 2019,64(3):729-739.
[32] Wong DM, Tam V, Lam R , et al. Protease-activated receptor 2 has pivotal roles in cellular mechanisms involved in experimental periodontitis[J]. Infect Immun, 2010,78(2):629-638.
[33] Kempuraj D, Selvakumar GP, Thangavel R , et al. Glia maturation factor and mast cell-dependent expression of inflammatory mediators and proteinase activated receptor-2 in neuroinflammation[J]. J Alzheimers Dis, 2018,66(3):1117-1129.
[34] Liu X, Wang J, Zhang H , et al. Induction of mast cell accumulation by tryptase via a protease activated receptor-2 and ICAM-1 dependent mechanism[J]. Mediators Inflamm, 2016,2016:6431574.
[35] An S, Zong G, Wang Z , et al. Activation of protease-activated receptor 4 of mast cells could downregulate proinflammatory cytokines in irritable bowel syndrome[J]. Gut, 2017,66(11):2040-2042.
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