Effects of HSP70 on TLR4 Expression by Increasing MAPK and NF-KB Signaling Pathways in Periodontitis

S. Shotorbani, Adel Espotin, J. Mahmoudi, A. Dehghan, S. S. Eteghad
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Abstract

Introduction: According to previous studies, heat shock protein 70 (HSP70) plays a role in the production of proinflammatory cytokines and inflammation. Given that no study has been performed in the field of dentistry in this regard, the present research aimed to identify the effect of HSP70 on moderate to severe generalized chronic periodontitis with the increase of mitogen-activated protein kinase (MAPK) and toll-like receptor 4 (TLR4) signaling pathways. Materials and Methods: This pilot study was performed on 50 subjects with moderate to severe chronic generalized periodontitis and 50 subjects with healthy periodontitis who were candidates for crown lengthening (CL) surgery. The subjects were selected based on the inclusion criteria from the patients who referred to the Gingival Surgery Department in a Private Dental Center, Tabriz, Iran. Tissue samples were obtained from the patients during pocket depth reduction surgery (for the experimental group) and CL surgery (for the control group). Macrophage inflammatory cells were extracted from tissue samples and the cells were stimulated by HSP70 as a timer; subsequently, the level of TLR4 in macrophage cells was examined. Results of the study were reported using descriptive statistical methods, such as mean, standard deviation, and frequency percentage. Repeated measures analysis was used to compare the expression of TLR4 in nuclear factor kappa B (NF-KB) and MAPK pathways at different hours. Moreover, ANOVA analysis of covariance was used to compare this rate between these two pathways at different times. Statistical analysis was performed in SPSS software (version 17) and a p -value of Results: Based on the results, there was a significant relationship between TLR4 and HSP70 (p <0.0001). It was also found that TLR4, MAPK, and NF-KB levels increased in the presence of HSP70. Conclusion: According to the findings, it can be said that TLR4 expression levels increased in the presence of HSP70 in periodontitis and can increase even more by excitation of MAPK and NF-KB pathways.
HSP70通过增加MAPK和NF-KB信号通路对牙周炎中TLR4表达的影响
前期研究发现,热休克蛋白70 (heat shock protein 70, HSP70)在促炎细胞因子的产生和炎症反应中发挥作用。鉴于目前在牙科领域尚未有相关研究,本研究旨在确定HSP70通过增加丝裂原活化蛋白激酶(MAPK)和toll样受体4 (TLR4)信号通路对中重度广泛性慢性牙周炎的影响。材料和方法:本初步研究纳入了50名中重度慢性广泛性牙周炎患者和50名健康牙周炎患者,这些患者都是牙冠延长(CL)手术的候选人。受试者是根据纳入标准从转诊到伊朗大不里士(Tabriz)一家私人牙科中心牙龈外科的患者中选择的。实验组和对照组分别进行口袋深度缩小手术和CL手术。从组织样本中提取巨噬细胞炎性细胞,用HSP70刺激细胞作为计时器;随后检测巨噬细胞中TLR4的表达水平。研究结果采用描述性统计方法报告,如平均值、标准差和频率百分比。采用重复测量分析比较不同时间TLR4在核因子κ B (NF-KB)和MAPK通路中的表达。此外,采用协方差的方差分析来比较这两种途径在不同时间的这一比率。采用SPSS软件(version 17)进行统计学分析,结果的p值为:基于结果,TLR4与HSP70之间存在显著相关(p <0.0001)。我们还发现,在HSP70存在的情况下,TLR4、MAPK和NF-KB水平升高。结论:根据研究结果,可以说在牙周炎中HSP70存在时,TLR4的表达水平升高,并且可以通过激发MAPK和NF-KB途径进一步升高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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审稿时长
12 weeks
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