miR-208 inhibits mitochondrial cardiomyocyte respiration in diabetic patients by inhibiting cytochrome C oxidase expression - 26/03/18
Résumé |
Introduction |
Diabetes is a common disease that is characterized by myocardial mitochondrial dysfunction. MicroRNAs are small non-coding RNAs that participate in the post-transcriptional regulation of many signaling pathways, and are involved in diabetes and mitochondrial function.
Objective |
The aim of this study was to investigate whether cardiac mitochondrial dysfunction observed in diabetic patients could be related to alteration in non-coding RNAs as suggested in bench-side studies.
Method |
A study of the non-coding transcriptome by microarrays was performed on 16 matched pairs of atrial myocardial samples from diabetic and non-diabetic patients who underwent aortic valve replacement and/or coronary artery bypass graft surgery at Lille University Hospital. Mitochondrial respiration in myocardial homogenates and expression of microRNAs identified by the transcriptomic analysis were studied in myocardial samples from a second population.
Results |
Analysis of the non-coding transcriptome revealed four microRNAs significantly deregulated in diabetic patients and predicted to target mitochondrial oxidative phosphorylation gene transcripts by bioinformatic analysis, i.e. miR-208, miR-4738, miR-498 and miR-1. Interestingly, in line with the predicted interaction between miR-208 and cytochrome C oxidase transcript, a significant negative correlation was observed between this miR expression level and complex IV-dependent mitochondrial respiration and complex activity (Fig. 1).
Conclusion |
miR-208 is likely linked to decreased cardiac expression of cytochrome c oxidase and subsequent depressed complex IV-dependent mitochondrial respiration in the myocardium of diabetic patients.
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Vol 10 - N° 2
P. 251 - avril 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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