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miR-21调控PTEN/PI3K/Akt通路抑制增生性瘢痕形成的机制研究 被引量:4

Mechanism of miR-21 Inhibiting Human Hypertrophic Scar Formation by Regulating PTEN/PI3K/Akt Pathway
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摘要 目的:探讨miR-21对增生性瘢痕中PTEN表达和成纤维细胞增殖的影响,以期为增生性瘢痕的临床诊断和治疗提供新靶点。方法:分别用qPCR和Westernblot检测增生性瘢痕(HTS)组织和细胞中miR-21及PTEN的表达;双荧光素酶报告基因检测验证miR-21与PTEN的调控关系;Westernblot检测miR-21对增生性瘢痕成纤维细胞(HSF)中PTEN蛋白表达影响;MTT检测细胞增殖能力变化。结果:HTS组织中miR-21高表达,PTEN低表达;双荧光素酶报告实验和Westernblot证实了miR-21对PTEN的靶向调控作用;下调miR-21可增加PTEN的表达,从而可抑制PI3K/Akt通路活性,抑制HSF细胞增殖。结论:本研究证实了miR-21具有诊断和治疗HTS的潜能,并为临床提供可能的新靶点。 Objective To investigate the effect of miR-21 on PTEN expression and fibroblast proliferation in hypertrophic scar, in order to provide a new target for clinical diagnosis and treatment of hypertrophic scar. Methods The expression of miR-21 and PTEN in HTS tissues and cells were detected by qPCR and western blot, respectively. Dual luciferase reporter gene assay to verify the regulatory relationship between miR-21 and PTEN. Western blot analysis of the effect of miR-21 on the expression of PTEN protein in HSF cells. MTT assay for cell proliferation. Results High expression of miR-21 and low expression of PTEN in HTS tissues. Dual luciferase reporter assay and western blot confirmed the targeted regulation of miR-21 on PTEN. Down-regulation of miR-21 inhibits PI3K/Akt pathway activity and up-regulates HSF cell proliferation by up-regulating PTEN expression. Conclusion This study demonstrates the potential of miR-21 to diagnose and treat HTS and may provide new targets for clinical use.
作者 史敏 李娜 郭晓波 魏超鹏 刘兆旺 封兴华 SHI Min;LI Na;GUO Xiao-bo;WEI Chao-peng;LIU Zhao-wang;FENG Xing-hua(Xi’an Peihua university,Xi’an 710125,Shaanxi,China;Department of Dermatology,Huayi Aesthetic Hospital,Xi’an 710061,Shaanxi,China;Clinical Laboratory,Xi’an Central Hospital,Xi’an 710003,Shaanxi,China)
出处 《中国美容医学》 CAS 2019年第3期92-95,共4页 Chinese Journal of Aesthetic Medicine
基金 2018年西安培华学院校级科研重点项目(miR-21调控PTEN/PI3K/AKt通路抑制人增生性瘢痕形成的机制研究 编号:PHKT18014)
关键词 MIR-21 PTEN 增生性瘢痕 HSF 细胞外基质 PI3K/Akt miR-21 PTEN hypertrophic scars hypertrophic scar fibroblasts extracellular matrix PI3K/Akt
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