Micro RNA-411 Expression Improves Cardiac Phenotype Following Myocardial Infarction in Mice.
CVEC, cardiac vascular endothelial cells
EdU, 5-ethynyl-2'-deoxyuridine
Hippo pathway
LAD, left anterior descending coronary artery
MI, myocardial infarction
MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide
NFAT, nuclear factor of activated T cells
NRCF, neonatal rat cardiac fibroblast
NRCM, neonatal rat cardiomyocytes
PCR, polymerase chain reaction
PEI, polyethylenimine
cTnI, cardiac troponin I
cardiac remodeling
heart failure
miRNA, microRNA
microRNA-411
myocardial infarction
pHH3, phosphohistone H3
qPCR, quantitative PCR
Journal
JACC. Basic to translational science
ISSN: 2452-302X
Titre abrégé: JACC Basic Transl Sci
Pays: United States
ID NLM: 101677259
Informations de publication
Date de publication:
Sep 2022
Sep 2022
Historique:
received:
07
09
2021
revised:
13
05
2022
accepted:
16
05
2022
entrez:
1
11
2022
pubmed:
2
11
2022
medline:
2
11
2022
Statut:
epublish
Résumé
Induction of endogenous regenerative capacity has emerged as one promising approach to repair damaged hearts following myocardial infarction (MI). Re-expression of factors that are exclusively expressed during embryonic development may reactivate the ability of adult cardiomyocytes to regenerate. Here, we identified miR-411 as a potent inducer of cardiomyocyte proliferation. Overexpression of miR-411 in the heart significantly increased cardiomyocyte proliferation and survival in a model MI. We found that miR-411 enhances the activity of YAP, the main downstream effector of the Hippo pathway, in cardiomyocytes. In conclusion, miR-411 induces cardiomyocyte regeneration and improves cardiac function post-MI likely by modulating the Hippo/YAP pathway.
Identifiants
pubmed: 36317138
doi: 10.1016/j.jacbts.2022.05.008
pii: S2452-302X(22)00215-7
pmc: PMC9617134
doi:
Types de publication
Journal Article
Langues
eng
Pagination
859-875Subventions
Organisme : Medical Research Council
ID : MR/P015816/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/17/78/33304
Pays : United Kingdom
Informations de copyright
© 2022 The Authors.
Déclaration de conflit d'intérêts
This study was supported by British Heart Foundation Project and Programme grants [PG/17/78/33304 and RG/F/21/110055 to Dr Oceandy] and a Medical Research Council research grant [MR/P015816/1 to Dr Oceandy]. Dr Nugroho was supported by an Indonesian LPDP (Lembaga Pengelola Dana Pendidikan/Indonesia Endowment Funds for Education) PhD scholarship (S-476/LPDP.3/2016). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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