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Epigenetic control of exercise training-induced cardiac hypertrophy by miR-208

2016; Portland Press; Volume: 130; Issue: 22 Linguagem: Inglês

10.1042/cs20160480

1470-8736

Úrsula Paula Renó Soci, Tiago Fernandes, Valério Garrone Baraúna, Nara Yumi Hashimoto, Glória de Fátima Alves da Mota, Kaleizu Teodoro Rosa, Maria Cláudia Irigoyen, Michael Ian Philips, Edilamar Menezes de Oliveira,

Circular RNAs in diseases

Aerobic exercise-induced cardiac hypertrophy (CH) is a physiological response involving accurate orchestration of gene and protein expression of contractile and metabolic components. The microRNAs: miR-208a, miR-208b and miR-499 are each encoded by a myosin gene and thus are also known as 'MyomiRs', regulating several mRNA targets that in turn regulate CH and metabolic pathways. To understand the role of myomiRs in the fine-tuning of cardiac myosin heavy chain (MHC) isoform expression by exercise training-induced physiological hypertrophy, Wistar rats were subjected to two different swim training protocols. We observed that high-volume swim training (T2), improved cardiac diastolic function, induced CH and decreased the expression of miR-208a and miR-208b Consequently, the increased expression of their targets, sex determining region y-related transcription factor 6 (Sox6), Med13, Purβ, specificity proteins (Sp)/Krüppel-like transcription factor 3 (SP3) and HP1β (heterochromatin protein 1β) was more prominent in T2, thus converging to modulate cardiac metabolic and contractile adaptation by exercise training, with an improvement in the α-MHC/β-MHC ratio, bypassing the increase in PPARβ and histone deacetylase (HDAC) class I and II regulation. Altogether, we conclude that high-volume swim training finely assures physiological cardiac remodelling by epigenetic regulation of myomiRs, because inhibition of miR-208a and miR-208b increases the expression of their target proteins and stimulates the interaction among metabolic, contractile and epigenetic genes.