Long noncoding RNA LINC01215 represses differentiation and proliferation of keratinocytes via zinc finger 652 in atopic dermatitis

IF 2.5 4区综合性期刊 Q2 MULTIDISCIPLINARY SCIENCES

Journal of Radiation Research and Applied Sciences Pub Date : 2025-06-05 DOI:10.1016/j.jrras.2025.101669

Qian Li , Hao Li , Qipeng Wei , Dongling Cai , Shiyu Lin , Xuting Zhang , Shiqing Deng , Jincheng Liu , Zhen Xiang , Wenxuan Dong , Chuanjian Lu , Xiaofeng Chen

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引用次数: 0

Abstract

Objective

Atopic dermatitis (AD) is a prevalent inflammatory disorder with high morbidity and seriously affects modern people. The pathogenesis of AD is complicated and involves multiple molecules. Long noncoding RNAs (lncRNAs) and zinc finger (ZNF) transcriptional factor (TF) are both essential regulators in various cellular processes. However, the roles of lncRNA LINC01215 and ZNF652 in the modulation of AD progression remain unclear. This study aims to explore the impact of LINC01215 and ZNF652 on AD.

Methods

HaCaT cells were treated with interferon-γ (IFN-γ) and anti-Fas antibody (anti-Fas-ab) to establish AD model in vitro. RNA immunoprecipitation (RIP) was used to identify the association between lncRNA and protein, while the interaction of protein and promoter was determined by chromatin immunoprecipitation (ChIP).

Results

LINC01215 and ZNF652 should suppress differentiation of keratinocytes by downregulating FLG. Mechanically, LINC01215 suppresses FLG gene transcription by recruiting ZNF652 to FLG gene promoter. Additionally, the depletion of LINC01215 and ZNF652 inhibit proliferation of HaCaT cells in AD model in vitro.

Conclusions

LINC01215 suppresses differentiation mediated by FLG and proliferation of keratinocytes via ZNF652 in AD. Our findings might provide novel targets for AD treatment.

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长链非编码RNA LINC01215通过锌指652抑制角化细胞在特应性皮炎中的分化和增殖

目的特应性皮炎（AD）是一种发病率高、严重影响现代人的常见病。AD的发病机制复杂，涉及多分子。长链非编码rna （lncRNAs）和锌指（ZNF）转录因子（TF）都是多种细胞过程的重要调控因子。然而，lncRNA LINC01215和ZNF652在AD进展调节中的作用尚不清楚。本研究旨在探讨LINC01215和ZNF652对AD的影响。方法用干扰素-γ (IFN-γ)和抗fas抗体（anti-Fas-ab）处理shaacat细胞，建立体外AD模型。采用RNA免疫沉淀法（RIP）鉴定lncRNA与蛋白的关联，采用染色质免疫沉淀法（ChIP）鉴定蛋白与启动子的相互作用。结果linc01215和ZNF652可能通过下调FLG抑制角质形成细胞的分化。机制上，LINC01215通过招募ZNF652到FLG基因启动子来抑制FLG基因的转录。此外，LINC01215和ZNF652的缺失可抑制体外AD模型HaCaT细胞的增殖。结论linc01215通过ZNF652抑制AD中FLG介导的分化和角质形成细胞的增殖。我们的发现可能为阿尔茨海默病的治疗提供新的靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Radiation Research and Applied Sciences MULTIDISCIPLINARY SCIENCES-

自引率

5.90%

发文量

130

审稿时长

16 weeks

期刊介绍： Journal of Radiation Research and Applied Sciences provides a high quality medium for the publication of substantial, original and scientific and technological papers on the development and applications of nuclear, radiation and isotopes in biology, medicine, drugs, biochemistry, microbiology, agriculture, entomology, food technology, chemistry, physics, solid states, engineering, environmental and applied sciences.