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微小RNA-31过表达可能通过STAT3/p53信号通路加重银屑病样皮损的形成。

MicroRNA-31 Overexpression may Aggravate the Formation of Psoriasis-like Lesions by STAT3/p53 Pathway.

作者信息

Wang Qiang, Wang Chunfang, Zhao Xincheng, Li Xiao, Li Junqin, Hou Ruixia, Yin Guohua, Zhang Kaiming

机构信息

ShanXi Key Laboratory of Stem Cell for Immunological Dermatosis, Institute of Dermatology, Taiyuan central Hospital of Shanxi Medical University, No. 5 Dong San Dao Xiang, Jiefang Road, Taiyuan, China.

ShanXi Medical University, No. 56, Xinjiannan Road, Taiyuan, ShanXi, China.

出版信息

Indian J Dermatol. 2021 Nov-Dec;66(6):598-603. doi: 10.4103/ijd.ijd_10_21.

DOI:10.4103/ijd.ijd_10_21
PMID:35283536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8906324/
Abstract

BACKGROUND

Psoriasis is a chronic inflammatory skin disease with an unknown pathogenesis. Recently, miR-31 have been shown to play an important role in psoriasis. Moreover, STAT3/p53 pathway has been used in tumor studies, but rarely in psoriasis studies.

AIMS

The present study aimed to investigate the role of STAT3/p53 pathway in psoriasis-like lesions in a mouse model of miR-31 overexpression.

METHODS

All mice (n = 44) were divided into four groups: normal mice treated with Vaseline® (NV; n = 10), normal mice treated with imiquimod (NI; n = 12), miR-31-overexpressing mice treated with Vaseline® (MV; n = 10), and miR-31-overexpressing mice treated with imiquimod (MI; n = 12). Then, we assayed the expression of STAT3 and p53.

RESULTS

Our results showed that at the protein level ( < 0.01) and gene level (4.45 times), the expression of STAT3 in the MV group was higher than that in the NV group, and at the protein level ( < 0.01) and gene level (11.43 times), the expression of STAT3 in the MI group was higher than that in the NI group. At the protein level, the expression of p53 in MV group was higher than that in the NV group ( < 0.05), and the expression of p53 in MI group was higher than that in the NI group ( < 0.01).

CONCLUSIONS

Our findings indicate that overexpression of miR-31 causes upregulation of STAT3, which further brings about upregulation of p53, and eventually leads to serious psoriasis skin lesion.

摘要

背景

银屑病是一种发病机制不明的慢性炎症性皮肤病。最近,miR-31已被证明在银屑病中起重要作用。此外,STAT3/p53通路已用于肿瘤研究,但在银屑病研究中很少使用。

目的

本研究旨在探讨STAT3/p53通路在miR-31过表达小鼠模型中银屑病样病变中的作用。

方法

将所有小鼠(n = 44)分为四组:用凡士林治疗的正常小鼠(NV;n = 10)、用咪喹莫特治疗的正常小鼠(NI;n = 12)、用凡士林治疗的miR-31过表达小鼠(MV;n = 10)和用咪喹莫特治疗的miR-31过表达小鼠(MI;n = 12)。然后,我们检测了STAT3和p53的表达。

结果

我们的结果显示,在蛋白水平(<0.01)和基因水平(4.45倍),MV组中STAT3的表达高于NV组,在蛋白水平(<0.01)和基因水平(11.43倍),MI组中STAT3的表达高于NI组。在蛋白水平上,MV组中p53的表达高于NV组(<0.05),MI组中p53的表达高于NI组(<0.01)。

结论

我们的研究结果表明,miR-31的过表达导致STAT3上调,进而导致p53上调,并最终导致严重的银屑病皮肤病变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/dfec698a563f/IJD-66-598-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/fd6fd61bfda0/IJD-66-598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/44b786a7fda3/IJD-66-598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/d8d0d2d42592/IJD-66-598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/c94124291028/IJD-66-598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/dfec698a563f/IJD-66-598-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/fd6fd61bfda0/IJD-66-598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/44b786a7fda3/IJD-66-598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/d8d0d2d42592/IJD-66-598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/c94124291028/IJD-66-598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8f26/8906324/dfec698a563f/IJD-66-598-g005.jpg

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