MicroRNA-26a及其靶基因Smad2在抑制增生性瘢痕形成中的作用

吴杨炀; 曹玲; 张霞; 祁俊

doi:10.16016/j.1000-5404.201908063

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MicroRNA-26a及其靶基因Smad2在抑制增生性瘢痕形成中的作用

基础医学 | 更新时间：2026-01-09

- MicroRNA-26a及其靶基因Smad2在抑制增生性瘢痕形成中的作用
- MicroRNA26a inhibits hyperplastic scar formation by targeting Smad2
- 第三军医大学学报 2020年42卷第2期页码：148-153
- 作者机构：
  
  1.226001 江苏南通，南通大学医学院护理系
  2.226001 江苏南通，南通大学附属医院烧伤整形科
- 作者简介：
  
  [祁俊，E-mail:qijunsky@126.com QI Jun, E-mail:qijunsky@126.com
- 基金信息：
- DOI：10.16016/j.1000-5404.201908063
  中图分类号： R394.2;R446.69;R619.6
- 收稿：2019-08-09，
  
  修回：2019-10-10，
  
  纸质出版：2020-01-30
- 稿件说明：
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吴杨炀, 曹玲, 张霞, 等. MicroRNA-26a及其靶基因Smad2在抑制增生性瘢痕形成中的作用[J]. 第三军医大学学报, 2020,42(2):148-153.

Yangyang WU, Ling CAO, Xia ZHANG, et al. MicroRNA26a inhibits hyperplastic scar formation by targeting Smad2[J]. Journal of Third Military Medical University, 2020, 42(2): 148-153.
吴杨炀, 曹玲, 张霞, 等. MicroRNA-26a及其靶基因Smad2在抑制增生性瘢痕形成中的作用[J]. 第三军医大学学报, 2020,42(2):148-153. DOI： 10.16016/j.1000-5404.201908063.

Yangyang WU, Ling CAO, Xia ZHANG, et al. MicroRNA26a inhibits hyperplastic scar formation by targeting Smad2[J]. Journal of Third Military Medical University, 2020, 42(2): 148-153. DOI： 10.16016/j.1000-5404.201908063.

摘要

目的

探讨microRNA-26a(miR-26a)及靶基因Smad2(mothers against decapentaplegic homolog 2)在增生性瘢痕(hypertrophic scar，HS)中的表达情况，以及在HS形成中可能发挥的作用。

方法

选取20例患者(年龄17~58岁; 女性13例，男性7例)，均接受过瘢痕切除及自体皮肤移植，获取的20对HS和正常皮肤组织(NS)，以及人胚胎皮肤成纤维细胞(CCC-ESF-1)和人HS成纤维细胞(hHSF)等，采用RT-qPCR和Western blot检测HS和NS中miR-26a的表达，统计分析miR-26a、Smad2与HS的相关性，利用双荧光素酶报告系统验证Smad2是否为miR-26a的靶基因；通过过表达和干扰Smad2，用RT-qPCR和Western blot检测ColⅠ和ColⅢ表达的变化。

结果

HS组织和hHSF中miR-26a的表达水平显著低于NS(

0.05)，在HS组织和hHSF细胞中Smad2表达显著升高(

0.05)；miR-26a能够靶向调节Smad2活性；Smad2过表达和敲低分别促进和抑制ColⅠ和ColⅢ的表达。

结论

HS患者中低表达的miR-26a可能通过上调靶基因Smad2，参与HS形成。

Abstract

Objective

To investigate the expression of microRNA-26a (mir-26a) and its target gene mothers against decapentaplegic homolog 2 (Smad2) in hypertrophic scar (HS) and explore their possible roles in HS formation.

Methods

Twenty patients (including 13 female and 7 male patients aged 17~58 years) previously receiving scar excision and autologous skin grafting were enrolled in this study. Real-time qPCR and Western blotting were performed for detecting the expression of miR-26a and Smad2 in the HS tissues and paired normal skin (NS) tissues obtained from the patients and in human skin fibroblasts (CCC-ESF-1) and HS fibroblasts (hHSFs). A dual luciferase reporting system was used to verify whether Smad2 was the target gene of miR-26a. The changes in Col Ⅰ and Col Ⅲ in hHSFs in response to over-expression and interference of Smad2 were examined using RT-qPCR and Western blotting.

Results

The expression level of miR-26a was significantly lower and that of Smad2 was significantly higher in HS tissues and hHSF than in NS tissues (

0.05). Dual luciferase assay confirmed that miR-26a could target Smad2 to regulate the activity of the latter. Smad2 overexpression and knockdown obviously promoted and inhibited

respectively

the expression of Col Ⅰ and Col Ⅲ in hHSFs.

Conclusion

A low expression of miR-26a may contribute to the formation of HS by up-regulating its target gene Smad2.

关键词

Keywords

references

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