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特发性肺纤维化患者肺成纤维细胞中lncRNA-mRNA共表达及调控分析

lncRNA-mRNA Co-Expression and Regulation Analysis in Lung Fibroblasts from Idiopathic Pulmonary Fibrosis.

作者信息

López-Martínez Armando, Santos-Álvarez Jovito Cesar, Velázquez-Enríquez Juan Manuel, Ramírez-Hernández Alma Aurora, Vásquez-Garzón Verónica Rocío, Baltierrez-Hoyos Rafael

机构信息

Laboratorio de Fibrosis y Cáncer, Facultad de Medicina y Cirugía, Universidad Autónoma Benito Juárez de Oaxaca, Ex Hacienda de Aguilera S/N, Sur, San Felipe del Agua, Oaxaca C.P. 68020, Mexico.

CONACYT-Facultad de Medicina y Cirugía, Universidad Autónoma Benito Juárez de Oaxaca, Ex Hacienda de Aguilera S/N, Sur, San Felipe del Agua, Oaxaca C.P. 68020, Mexico.

出版信息

Noncoding RNA. 2024 Apr 17;10(2):26. doi: 10.3390/ncrna10020026.

DOI:10.3390/ncrna10020026
PMID:38668384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11054336/
Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease marked by abnormal accumulation of extracellular matrix (ECM) due to dysregulated expression of various RNAs in pulmonary fibroblasts. This study utilized RNA-seq data meta-analysis to explore the regulatory network of hub long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) in IPF fibroblasts. The meta-analysis unveiled 584 differentially expressed mRNAs (DEmRNA) and 75 differentially expressed lncRNAs (DElncRNA) in lung fibroblasts from IPF. Among these, BCL6, EFNB1, EPHB2, FOXO1, FOXO3, GNAI1, IRF4, PIK3R1, and RXRA were identified as hub mRNAs, while AC008708.1, AC091806.1, AL442071.1, FAM111A-DT, and LINC01989 were designated as hub lncRNAs. Functional characterization revealed involvement in TGF-β, PI3K, FOXO, and MAPK signaling pathways. Additionally, this study identified regulatory interactions between sequences of hub mRNAs and lncRNAs. In summary, the findings suggest that AC008708.1, AC091806.1, FAM111A-DT, LINC01989, and AL442071.1 lncRNAs can regulate BCL6, EFNB1, EPHB2, FOXO1, FOXO3, GNAI1, IRF4, PIK3R1, and RXRA mRNAs in fibroblasts bearing IPF and contribute to fibrosis by modulating crucial signaling pathways such as FoxO signaling, chemical carcinogenesis, longevity regulatory pathways, non-small cell lung cancer, and AMPK signaling pathways.

摘要

特发性肺纤维化（IPF）是一种进行性肺部疾病，其特征是由于肺成纤维细胞中各种RNA表达失调，导致细胞外基质（ECM）异常积累。本研究利用RNA测序数据的荟萃分析来探索IPF成纤维细胞中关键长链非编码RNA（lncRNA）和信使RNA（mRNA）的调控网络。荟萃分析揭示了IPF肺成纤维细胞中有584个差异表达的mRNA（DEmRNA）和75个差异表达的lncRNA（DElncRNA）。其中，BCL6、EFNB1、EPHB2、FOXO1、FOXO3、GNAI1、IRF4、PIK3R1和RXRA被鉴定为关键mRNA，而AC008708.1、AC091806.1、AL442071.1、FAM111A-DT和LINC01989被指定为关键lncRNA。功能表征显示其参与了转化生长因子-β（TGF-β）、磷脂酰肌醇-3激酶（PI3K）、叉头框蛋白O（FOXO）和丝裂原活化蛋白激酶（MAPK）信号通路。此外，本研究还确定了关键mRNA和lncRNA序列之间的调控相互作用。总之，研究结果表明，AC008708.1、AC091806.1、FAM111A-DT、LINC01989和AL442071.1 lncRNA可以调节IPF成纤维细胞中的BCL6、EFNB1、EPHB2、FOXO1、FOXO3、GNAI1、IRF4、PIK3R1和RXRA mRNA，并通过调节诸如FoxO信号通路、化学致癌作用、长寿调节通路、非小细胞肺癌和AMPK信号通路等关键信号通路来促进纤维化。

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