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4 décembre 2017
- doi: 10.1038/s41598-017-16829-w
- issn: 2045-2322
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info:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-017-16829-w
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info:eu-repo/semantics/altIdentifier/pmid/29203887
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info:eu-repo/semantics/altIdentifier/eissn/2045-2322
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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_219FB1ADDEA86
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
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J. Heid et al., « Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health. », Serveur académique Lausannois, ID : 10.1038/s41598-017-16829-w
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The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12-21 week (adult) and 28-40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O 2 levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.