[1]张鼎伟,王媛,霍佳,等.miR-142-3p/Sema3A轴调节角质形成细胞增殖凋亡及银屑病皮肤炎症反应[J].中国皮肤性病学杂志,2021,(02):127-132.
 ZHANG Dingwei,WANG Yuan,HUO Jia,et al.miR-142-3p/Sema3A Axis Modulates Proliferation and Apoptosis of Keratinocytes and Skin Inflammation in Psoriasis[J].The Chinese Journal of Dermatovenereology,2021,(02):127-132.
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miR-142-3p/Sema3A轴调节角质形成细胞增殖凋亡及银屑病皮肤炎症反应()
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《中国皮肤性病学杂志》[ISSN:1001-7089/CN:61-1197/R]

卷:
期数:
2021年02期
页码:
127-132
栏目:
论著
出版日期:
2021-02-01

文章信息/Info

Title:
miR-142-3p/Sema3A Axis Modulates Proliferation and Apoptosis of Keratinocytes and Skin Inflammation in Psoriasis
文章编号:
1001-7089(2021)02-0127-06
作者:
张鼎伟王媛霍佳汪炜彭斌张燕飞
西安交通大学医学院第二附属医院皮肤科,陕西 西安 710004
Author(s):
ZHANG DingweiWANG YuanHUO JiaWANG WeiPENG BinZHANG Yanfei
(Department of Dermatology,the Second Affiliated Hospital of Xi'an Jiaotong University Medical College,Xi'an 710004, China)
关键词:
MiR-142-3p 异常增殖 炎症反应 Sema3A 银屑病
Keywords:
miR-142-3p Hyperproliferation Inflammation Sema3A Psoriasis
分类号:
R 758.63
文献标志码:
A
摘要:
目的 旨在探讨miR-142-3p在M5刺激人表皮角质形成细胞HaCaT中的作用及潜在机制。方法 MTT法检测细胞增殖; ELISA凋亡检测试剂盒评估细胞凋亡。ELISA试剂盒测定炎症介质TNF-α、IL-22和IL-17A的分泌量。RT-PCR和Western blot分别测定目的基因mRNA和蛋白表达。荧光素酶报告实验评估荧光素酶活性。结果 M5刺激的HaCaT细胞中miR-142-3p表达升高。下调miR-142-3p显著抑制M5诱导HaCaT细胞的增殖并促进凋亡,抗凋亡蛋白Bcl-2减少,伴随促凋亡蛋白Bax增加。此外,下调miR-142-3p通过降低多种炎症因子的表达改善M5诱导的炎症反应。重要的是,miR-142-3p负调控靶基因Sema3A的表达。从机制上讲,沉默Sema3A有效逆转miR-142-3p下调对HaCaT细胞的抗增殖、促凋亡及抗炎作用。结论 下调miR-142-3p通过调控靶基因Sema3A保护HaCaT细胞免受M5诱导的过度增殖和炎症损伤,揭示miR-142-3p/Sema3A轴可能是防止角质形成细胞损伤的新靶点。
Abstract:
Objective The aim of the present study was to explore the functions and precise mechanism of miR-142-3p in human keratinocyte HaCaT cells in the presence of M5.Methods CCK-8 assay was conducted to measure cell proliferation.Apoptosis was assessed using Cell Death Detection ELISAPLUS Kit.The concentrations of TNF-α,IL-22 and IL-17A were estimated using ELISA assays.RT-PCR and Western blot was applied to evaluate mRNA and protein expression,respectively.Luciferase activity was determined using a Dual-luciferase Reporter Assay.Results MiR-142-3p expression was heightened in HaCaT cells induced by M5.In addition,inhibition of miR-142-3p dramatically restricted cell proliferation and enhanced apoptosis in HaCaT cells exposed to M5,as exemplified by a decrease in the anti-apoptotic Bcl-2 protein,concomitant with an increase in the pro-apoptotic proteins Bax.Moreover,depleting miR-142-3p effectively ameliorated M5-induced inflammation response,as reflected by the attenuation of multiple inflammatory factors.Importantly,Sema3A was identified as a direct target of miR-142-3p,and negatively regulated by miR-142-3p.Mecha-nistically,silencing of Sema3A effectively abolished the anti-proliferative,apoptosis-promoting,and anti-inflammatory effects of miR-142-3p inhibition in keratinocytes.Conclusion Repression of miR-142-3p protected HaCaT cells against M5-induced hyper-proliferation and inflammatory injury by suppressing its target Sema3A,implying that the miR-142-3p/Sema3A axis may be a new target for preventing keratinocyte injury process.

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备注/Memo

备注/Memo:
[基金项目] 国家自然科学基金(81703129,81903214)
[通信作者] 张燕飞,E-mail:zhangyanfei723@163.com
更新日期/Last Update: 2021-02-01