Cargando…

Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis

In this study, we obtained the RNA expression data of murine skin tissues of control, and UVB irradiated groups. After the re-annotation of lncRNAs, a gene expression similarity analysis was done by WGCNA. The target mRNA prediction of lncRNAs, miRNAs, and ceRNA regulatory networks were constructed...

Descripción completa

Detalles Bibliográficos
Autores principales: Zhang, Nan, Zhong, Zhou, Wang, Yujia, Yang, Li, Wu, Fengbo, Peng, Cheng, Huang, Wei, He, Gu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914409/
https://www.ncbi.nlm.nih.gov/pubmed/31761787
http://dx.doi.org/10.18632/aging.102483
_version_ 1783479799539302400
author Zhang, Nan
Zhong, Zhou
Wang, Yujia
Yang, Li
Wu, Fengbo
Peng, Cheng
Huang, Wei
He, Gu
author_facet Zhang, Nan
Zhong, Zhou
Wang, Yujia
Yang, Li
Wu, Fengbo
Peng, Cheng
Huang, Wei
He, Gu
author_sort Zhang, Nan
collection PubMed
description In this study, we obtained the RNA expression data of murine skin tissues of control, and UVB irradiated groups. After the re-annotation of lncRNAs, a gene expression similarity analysis was done by WGCNA. The target mRNA prediction of lncRNAs, miRNAs, and ceRNA regulatory networks were constructed by five lncRNAs, 14 miRNAs and 54 mRNAs, respectively. Based on the ceRNA network of UVB-induced skin lesions, it was evident that the dysregulation of Meg3 has critical effects on the UVB-induced inflammatory lesion of murine skin tissues. The overexpression of Meg3 after UVB irradiation was observed in primary murine skin fibroblasts, and the up-regulated Meg3 expression was related to the activation of the inflammatory cytokines. These functional experiments demonstrated that the RNA silencing of Meg3 in murine skin fibroblasts could suppress the expression of the cytokines (in vitro) and UVB-induced skin lesions (in vivo). Moreover, the Meg3 functioned as a competing endogenous RNA (ceRNA) that acted as a sponge for miR-93-5p and thereby modulated the expression of Epiregulin (Ereg). Our results proved that Meg3 was involved in UVB-induced skin inflammation and that the ceRNA networks, which includes miR-93-5p and Ereg, could prove to be a potential therapeutic target for UVB-induced skin damage.
format Online
Article
Text
id pubmed-6914409
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher Impact Journals
record_format MEDLINE/PubMed
spelling pubmed-69144092019-12-19 Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis Zhang, Nan Zhong, Zhou Wang, Yujia Yang, Li Wu, Fengbo Peng, Cheng Huang, Wei He, Gu Aging (Albany NY) Research Paper In this study, we obtained the RNA expression data of murine skin tissues of control, and UVB irradiated groups. After the re-annotation of lncRNAs, a gene expression similarity analysis was done by WGCNA. The target mRNA prediction of lncRNAs, miRNAs, and ceRNA regulatory networks were constructed by five lncRNAs, 14 miRNAs and 54 mRNAs, respectively. Based on the ceRNA network of UVB-induced skin lesions, it was evident that the dysregulation of Meg3 has critical effects on the UVB-induced inflammatory lesion of murine skin tissues. The overexpression of Meg3 after UVB irradiation was observed in primary murine skin fibroblasts, and the up-regulated Meg3 expression was related to the activation of the inflammatory cytokines. These functional experiments demonstrated that the RNA silencing of Meg3 in murine skin fibroblasts could suppress the expression of the cytokines (in vitro) and UVB-induced skin lesions (in vivo). Moreover, the Meg3 functioned as a competing endogenous RNA (ceRNA) that acted as a sponge for miR-93-5p and thereby modulated the expression of Epiregulin (Ereg). Our results proved that Meg3 was involved in UVB-induced skin inflammation and that the ceRNA networks, which includes miR-93-5p and Ereg, could prove to be a potential therapeutic target for UVB-induced skin damage. Impact Journals 2019-11-24 /pmc/articles/PMC6914409/ /pubmed/31761787 http://dx.doi.org/10.18632/aging.102483 Text en Copyright © 2019 Zhang et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Zhang, Nan
Zhong, Zhou
Wang, Yujia
Yang, Li
Wu, Fengbo
Peng, Cheng
Huang, Wei
He, Gu
Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis
title Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis
title_full Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis
title_fullStr Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis
title_full_unstemmed Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis
title_short Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis
title_sort competing endogenous network analysis identifies lncrna meg3 activates inflammatory damage in uvb induced murine skin lesion by sponging mir-93-5p/epiregulin axis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6914409/
https://www.ncbi.nlm.nih.gov/pubmed/31761787
http://dx.doi.org/10.18632/aging.102483
work_keys_str_mv AT zhangnan competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis
AT zhongzhou competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis
AT wangyujia competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis
AT yangli competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis
AT wufengbo competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis
AT pengcheng competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis
AT huangwei competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis
AT hegu competingendogenousnetworkanalysisidentifieslncrnameg3activatesinflammatorydamageinuvbinducedmurineskinlesionbyspongingmir935pepiregulinaxis