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Anti-inflammatory effects of miRNA-146a induced in adipose and periodontal tissues

机译:脂肪和牙周组织中miRNA-146a的抗炎作用

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摘要

MicroRNA (miRNA) plays an important role in diverse cellular biological processes such as inflammatory response, differentiation and proliferation, and carcinogenesis. miR-146a has been suggested as a negative regulator of the inflammatory reaction. Although, it has been reported as expressed in inflamed adipose and periodontal tissues, however, miR-146a's inhibitory effects against inflammatory response in both the tissues, are not well understood. Therefore, in this study, the inhibitory effects of miR-146a on both adipose and periodontal inflammation, was investigated. study has revealed that miR-146a transfection into either adipocytes or gingival fibroblasts, has resulted in a reduced cytokine gene expression, observed on co-culturing the cells with macrophages in the presence of lipopolysaccharides (LPS), in comparison to the control miRNA transfected. Similarly, miR-146a transfection into macrophages resulted in a reduced expression of TNF-α gene and protein in response to LPS stimulation. study revealed that a continuous intravenous miR-146a administration into mice via tail vein, protected the mice from developing high-fat diet-induced obesity and the inflammatory cytokine gene expression was down-regulated in both adipose and periodontal tissues. miR-146a appeared to be induced by macrophage-derived inflammatory signals such as TNF-α by negative feed-back mechanism, and it suppressed inflammatory reaction in both adipose and periodontal tissues. Therefore, miR-146a could be suggested as a potential therapeutic molecule and as a common inflammatory regulator for both obesity-induced diabetes and related periodontal diseases.
机译:MicroRNA(miRNA)在多种细胞生物学过程中发挥重要作用,例如炎症反应,分化和增殖以及致癌作用。已建议将miR-146a作为炎症反应的负调节剂。尽管据报道它在发炎的脂肪和牙周组织中表达,但是,人们对miR-146a对两种组织中炎症反应的抑制作用的了解还不清楚。因此,在这项研究中,研究了miR-146a对脂肪和牙周炎症的抑制作用。研究表明,与转染的对照miRNA相比,在脂多糖(LPS)存在下将细胞与巨噬细胞共培养时,miR-146a转染到脂肪细胞或牙龈成纤维细胞中导致细胞因子基因表达降低。同样,将miR-146a转染至巨噬细胞后,响应LPS刺激,TNF-α基因和蛋白质的表达降低。研究表明,通过尾静脉向小鼠连续静脉内施用miR-146a可以保护小鼠免受高脂饮食诱导的肥胖的影响,并且脂肪和牙周组织中炎性细胞因子的基因表达均被下调。 miR-146a似乎是由巨噬细胞衍生的炎症信号(如TNF-α)通过负反馈机制诱导的,并且它抑制了脂肪和牙周组织的炎症反应。因此,miR-146a可能被建议作为肥胖引起的糖尿病和相关牙周疾病的潜在治疗分子和常见的炎症调节剂。

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