The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury

Background: Myocardial ischaemia/reperfusion (I/R) injury is still a major challenge in clinical treatment. The role of long non-coding RNA (lncRNA) in the regulation of myocardial I/R injury still needs to be elucidated.Methods: The primary isolated neonatal mousse cardiomyocytes and adult mice wer...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Zhaoyan Xu, Yuanxi Mo, Xinyi Li, Wanzi Hong, Sisi Shao, Yaoxin Liu, Fen Shu, Lei Jiang, Ning Tan
Formato: article
Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://doaj.org/article/9f1482b4c57a446094c97d7b20bfd1a0
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:9f1482b4c57a446094c97d7b20bfd1a0
record_format dspace
spelling oai:doaj.org-article:9f1482b4c57a446094c97d7b20bfd1a02021-11-08T05:41:33ZThe Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury2296-634X10.3389/fcell.2021.773381https://doaj.org/article/9f1482b4c57a446094c97d7b20bfd1a02021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.773381/fullhttps://doaj.org/toc/2296-634XBackground: Myocardial ischaemia/reperfusion (I/R) injury is still a major challenge in clinical treatment. The role of long non-coding RNA (lncRNA) in the regulation of myocardial I/R injury still needs to be elucidated.Methods: The primary isolated neonatal mousse cardiomyocytes and adult mice were used to construct a myocardial ischemia-reperfusion model. qRT-PCR is used to verify gene expression in myocardial tissue and myocardial cells. The effect of AK035396 in primary cardiomyocytes and mouse myocardium was confirmed by TUNEL staining and in vitro flow cytometry experiments. RNA pulldown and Western blot were used to identify AK035396 interacting proteins. The expression of apoptosis-related proteins was identified by qRT-PCR and Western blot.Results:In vivo and in vitro MIRI models, AK035396 was up-regulated after myocardial infarction. Functional studies have shown that knockdown of AK035396 reduces the apoptosis of primary cardiomyocytes and mouse myocardial tissue. AK035396 directly interacts with Mterf1 and inhibits the level of Mterf1. Further experiments have shown that inhibiting Mterf1 will promote the expression of mitochondrial genes COXII and CYTb and cause cell apoptosis.Conclusion: AK035396 plays an important role in myocardial ischaemia-reperfusion injury by regulating the Mterf1-COXII/CYTb pathway.Zhaoyan XuYuanxi MoXinyi LiXinyi LiWanzi HongWanzi HongSisi ShaoSisi ShaoYaoxin LiuYaoxin LiuFen ShuFen ShuLei JiangLei JiangNing TanNing TanNing TanFrontiers Media S.A.articleMterf1apoptosisischemia/reperfusionlncRNAmitochondrial functionBiology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021)
institution DOAJ
collection DOAJ
language EN
topic Mterf1
apoptosis
ischemia/reperfusion
lncRNA
mitochondrial function
Biology (General)
QH301-705.5
spellingShingle Mterf1
apoptosis
ischemia/reperfusion
lncRNA
mitochondrial function
Biology (General)
QH301-705.5
Zhaoyan Xu
Yuanxi Mo
Xinyi Li
Xinyi Li
Wanzi Hong
Wanzi Hong
Sisi Shao
Sisi Shao
Yaoxin Liu
Yaoxin Liu
Fen Shu
Fen Shu
Lei Jiang
Lei Jiang
Ning Tan
Ning Tan
Ning Tan
The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury
description Background: Myocardial ischaemia/reperfusion (I/R) injury is still a major challenge in clinical treatment. The role of long non-coding RNA (lncRNA) in the regulation of myocardial I/R injury still needs to be elucidated.Methods: The primary isolated neonatal mousse cardiomyocytes and adult mice were used to construct a myocardial ischemia-reperfusion model. qRT-PCR is used to verify gene expression in myocardial tissue and myocardial cells. The effect of AK035396 in primary cardiomyocytes and mouse myocardium was confirmed by TUNEL staining and in vitro flow cytometry experiments. RNA pulldown and Western blot were used to identify AK035396 interacting proteins. The expression of apoptosis-related proteins was identified by qRT-PCR and Western blot.Results:In vivo and in vitro MIRI models, AK035396 was up-regulated after myocardial infarction. Functional studies have shown that knockdown of AK035396 reduces the apoptosis of primary cardiomyocytes and mouse myocardial tissue. AK035396 directly interacts with Mterf1 and inhibits the level of Mterf1. Further experiments have shown that inhibiting Mterf1 will promote the expression of mitochondrial genes COXII and CYTb and cause cell apoptosis.Conclusion: AK035396 plays an important role in myocardial ischaemia-reperfusion injury by regulating the Mterf1-COXII/CYTb pathway.
format article
author Zhaoyan Xu
Yuanxi Mo
Xinyi Li
Xinyi Li
Wanzi Hong
Wanzi Hong
Sisi Shao
Sisi Shao
Yaoxin Liu
Yaoxin Liu
Fen Shu
Fen Shu
Lei Jiang
Lei Jiang
Ning Tan
Ning Tan
Ning Tan
author_facet Zhaoyan Xu
Yuanxi Mo
Xinyi Li
Xinyi Li
Wanzi Hong
Wanzi Hong
Sisi Shao
Sisi Shao
Yaoxin Liu
Yaoxin Liu
Fen Shu
Fen Shu
Lei Jiang
Lei Jiang
Ning Tan
Ning Tan
Ning Tan
author_sort Zhaoyan Xu
title The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury
title_short The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury
title_full The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury
title_fullStr The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury
title_full_unstemmed The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury
title_sort novel lncrna ak035396 drives cardiomyocyte apoptosis through mterf1 in myocardial ischemia/reperfusion injury
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/9f1482b4c57a446094c97d7b20bfd1a0
work_keys_str_mv AT zhaoyanxu thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT yuanximo thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT xinyili thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT xinyili thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT wanzihong thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT wanzihong thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT sisishao thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT sisishao thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT yaoxinliu thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT yaoxinliu thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT fenshu thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT fenshu thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT leijiang thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT leijiang thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT ningtan thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT ningtan thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT ningtan thenovellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT zhaoyanxu novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT yuanximo novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT xinyili novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT xinyili novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT wanzihong novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT wanzihong novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT sisishao novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT sisishao novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT yaoxinliu novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT yaoxinliu novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT fenshu novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT fenshu novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT leijiang novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT leijiang novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT ningtan novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT ningtan novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
AT ningtan novellncrnaak035396drivescardiomyocyteapoptosisthroughmterf1inmyocardialischemiareperfusioninjury
_version_ 1718442931966181376