N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways

Lung ischemia-reperfusion injury (LIRI) is a common complication after lung transplantation, embolism, and trauma. N6-methyladenosine (m6A) methylation modification has been found to be implicated in the pathogenesis of ischemia/reperfusion injury. However, there are no or few reports of m6A-related...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Kun Xiao, Pengfei Liu, Peng Yan, Yanxin Liu, Licheng Song, Yuhong Liu, Lixin Xie
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	n6-methyladenosine ythdf3 igf2bp2 lung injury hypoxia reoxygenation Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/82f30ac06b1d4d98a590c629abdc3fec
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:82f30ac06b1d4d98a590c629abdc3fec
record_format	dspace
spelling	oai:doaj.org-article:82f30ac06b1d4d98a590c629abdc3fec2021-11-04T15:51:54ZN6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways2165-59792165-598710.1080/21655979.2021.1999550https://doaj.org/article/82f30ac06b1d4d98a590c629abdc3fec2021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1999550https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Lung ischemia-reperfusion injury (LIRI) is a common complication after lung transplantation, embolism, and trauma. N6-methyladenosine (m6A) methylation modification has been found to be implicated in the pathogenesis of ischemia/reperfusion injury. However, there are no or few reports of m6A-related regulators in LIRI till now. In this text, differentially expressed genes in lung tissues of LIRI rats versus the sham group were identified by RNA sequencing (RNA-seq). RNA-seq outcomes revealed that only YTH N6-methyladenosine RNA binding protein 3 (YTHDF3) and insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) were differentially expressed in the LIRI versus sham group among 20 m6A-related regulators. Next, the functions and molecular mechanisms of YTHDF3 and IGF2BP2 in LIRI were investigated in a hypoxia/reoxygenation-induced BEAS-2B cell injury model in vitro. Loss-of-function experiments demonstrated that YTHDF3 or IGF2BP2 knockdown attenuated hypoxia/reoxygenation-mediated inhibitory effects on cell survival and cell cycle progression and inhibited hypoxia/reoxygenation-induced cell apoptosis and pro-inflammatory cytokine secretion in BEAS-2B cells. Genes that could be directly regulated by YTHDF3 or IGF2BP2 were identified based on prior experimental data and bioinformatics analysis. Moreover, multiple potential downstream pathways of YTHDF3 and IGF2BP2 were identified by the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis of the above-mentioned genes. Among these potential pathways, we demonstrated that YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-κB pathways in BEAS-2B cells. In conclusion, YTHDF3 or IGF2BP2 knockdown weakened hypoxia/reoxygenation-induced human lung bronchial epithelial cell injury by inactivating p38, AKT, ERK1/2, and NF-κB pathways.Kun XiaoPengfei LiuPeng YanYanxin LiuLicheng SongYuhong LiuLixin XieTaylor & Francis Grouparticlen6-methyladenosineythdf3igf2bp2lunginjuryhypoxiareoxygenationBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	n6-methyladenosine ythdf3 igf2bp2 lung injury hypoxia reoxygenation Biotechnology TP248.13-248.65
spellingShingle	n6-methyladenosine ythdf3 igf2bp2 lung injury hypoxia reoxygenation Biotechnology TP248.13-248.65 Kun Xiao Pengfei Liu Peng Yan Yanxin Liu Licheng Song Yuhong Liu Lixin Xie N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways
description	Lung ischemia-reperfusion injury (LIRI) is a common complication after lung transplantation, embolism, and trauma. N6-methyladenosine (m6A) methylation modification has been found to be implicated in the pathogenesis of ischemia/reperfusion injury. However, there are no or few reports of m6A-related regulators in LIRI till now. In this text, differentially expressed genes in lung tissues of LIRI rats versus the sham group were identified by RNA sequencing (RNA-seq). RNA-seq outcomes revealed that only YTH N6-methyladenosine RNA binding protein 3 (YTHDF3) and insulin like growth factor 2 mRNA binding protein 2 (IGF2BP2) were differentially expressed in the LIRI versus sham group among 20 m6A-related regulators. Next, the functions and molecular mechanisms of YTHDF3 and IGF2BP2 in LIRI were investigated in a hypoxia/reoxygenation-induced BEAS-2B cell injury model in vitro. Loss-of-function experiments demonstrated that YTHDF3 or IGF2BP2 knockdown attenuated hypoxia/reoxygenation-mediated inhibitory effects on cell survival and cell cycle progression and inhibited hypoxia/reoxygenation-induced cell apoptosis and pro-inflammatory cytokine secretion in BEAS-2B cells. Genes that could be directly regulated by YTHDF3 or IGF2BP2 were identified based on prior experimental data and bioinformatics analysis. Moreover, multiple potential downstream pathways of YTHDF3 and IGF2BP2 were identified by the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis of the above-mentioned genes. Among these potential pathways, we demonstrated that YTHDF3 or IGF2BP2 knockdown inhibited hypoxia/reoxygenation-activated p38, ERK1/2, AKT, and NF-κB pathways in BEAS-2B cells. In conclusion, YTHDF3 or IGF2BP2 knockdown weakened hypoxia/reoxygenation-induced human lung bronchial epithelial cell injury by inactivating p38, AKT, ERK1/2, and NF-κB pathways.
format	article
author	Kun Xiao Pengfei Liu Peng Yan Yanxin Liu Licheng Song Yuhong Liu Lixin Xie
author_facet	Kun Xiao Pengfei Liu Peng Yan Yanxin Liu Licheng Song Yuhong Liu Lixin Xie
author_sort	Kun Xiao
title	N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways
title_short	N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways
title_full	N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways
title_fullStr	N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways
title_full_unstemmed	N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways
title_sort	n6-methyladenosine reader yth n6-methyladenosine rna binding protein 3 or insulin like growth factor 2 mrna binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 mapk, akt, erk1/2, and nf-κb pathways
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/82f30ac06b1d4d98a590c629abdc3fec
work_keys_str_mv	AT kunxiao n6methyladenosinereaderythn6methyladenosinernabindingprotein3orinsulinlikegrowthfactor2mrnabindingprotein2knockdownprotectshumanbronchialepithelialcellsfromhypoxiareoxygenationinjurybyinactivatingp38mapkakterk12andnfkbpathways AT pengfeiliu n6methyladenosinereaderythn6methyladenosinernabindingprotein3orinsulinlikegrowthfactor2mrnabindingprotein2knockdownprotectshumanbronchialepithelialcellsfromhypoxiareoxygenationinjurybyinactivatingp38mapkakterk12andnfkbpathways AT pengyan n6methyladenosinereaderythn6methyladenosinernabindingprotein3orinsulinlikegrowthfactor2mrnabindingprotein2knockdownprotectshumanbronchialepithelialcellsfromhypoxiareoxygenationinjurybyinactivatingp38mapkakterk12andnfkbpathways AT yanxinliu n6methyladenosinereaderythn6methyladenosinernabindingprotein3orinsulinlikegrowthfactor2mrnabindingprotein2knockdownprotectshumanbronchialepithelialcellsfromhypoxiareoxygenationinjurybyinactivatingp38mapkakterk12andnfkbpathways AT lichengsong n6methyladenosinereaderythn6methyladenosinernabindingprotein3orinsulinlikegrowthfactor2mrnabindingprotein2knockdownprotectshumanbronchialepithelialcellsfromhypoxiareoxygenationinjurybyinactivatingp38mapkakterk12andnfkbpathways AT yuhongliu n6methyladenosinereaderythn6methyladenosinernabindingprotein3orinsulinlikegrowthfactor2mrnabindingprotein2knockdownprotectshumanbronchialepithelialcellsfromhypoxiareoxygenationinjurybyinactivatingp38mapkakterk12andnfkbpathways AT lixinxie n6methyladenosinereaderythn6methyladenosinernabindingprotein3orinsulinlikegrowthfactor2mrnabindingprotein2knockdownprotectshumanbronchialepithelialcellsfromhypoxiareoxygenationinjurybyinactivatingp38mapkakterk12andnfkbpathways
_version_	1718444724043382784

N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-κB pathways

Ejemplares similares