Epigenetic control of exercise training-induced cardiac hypertrophy by <i>miR-208</i>

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

doi:10.1042/cs20160480

Cited by 54 publications

(43 citation statements)

References 40 publications

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“…Consistent with this, cardiac miR‐208b levels are known to be downregulated following endurance exercise (Soci et al . ). However, it is unlikely miR‐208b is responsible for the sustained increase in cardiomyocyte number since its current known function in the heart is the regulation of myosin heavy chain expression (Soci et al .…”

Section: Discussionmentioning

confidence: 97%

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Sustained cardiac programming by short‐term juvenile exercise training in male rats

Asif

Wlodek

Black

et al. 2017

The Journal of Physiology

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The aim of this study was to investigate if endurance training during juvenile life 'reprogrammes' the heart and leads to sustained improvements in the structure, function, and morphology of the adult heart. Male Wistar Kyoto rats were exercise trained 5 days week for 4 weeks in either juvenile (5-9 weeks of age), adolescent (11-15 weeks of age) or adult life (20-24 weeks of age). Juvenile exercise training, when compared to 24-week-old sedentary rats, led to sustained increases in left ventricle (LV) mass (+18%; P < 0.05), wall thickness (+11%; P < 0.05), the longitudinal area of binucleated cardiomyocytes (P < 0.05), cardiomyocyte number (+36%; P < 0.05), and doubled the proportion of mononucleated cardiomyocytes (P < 0.05), with a less pronounced effect of exercise during adolescent life. Adult exercise training also increased LV mass (+11%; P < 0.05), wall thickness (+6%; P < 0.05) and the longitudinal area of binucleated cardiomyocytes (P < 0.05), despite no change in cardiomyocyte number or the proportion of mono- and binucleated cardiomyocytes. Resting cardiac function, LV chamber dimensions and fibrosis levels were not altered by juvenile or adult exercise training. At 9 weeks of age, juvenile exercise significantly reduced the expression of microRNA-208b, which is a known regulator of cardiac growth, but this was not sustained to 24 weeks of age. In conclusion, juvenile exercise leads to physiological cardiac hypertrophy that is sustained into adulthood long after exercise training has ceased. Furthermore, this cardiac reprogramming is largely due to a 36% increase in cardiomyocyte number, which results in an additional 20 million cardiomyocytes in adulthood.

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Section: Discussionmentioning

confidence: 97%

“…However, it is unlikely miR‐208b is responsible for the sustained increase in cardiomyocyte number since its current known function in the heart is the regulation of myosin heavy chain expression (Soci et al . ; Zhou et al . ) and myh6 mRNA levels were unaltered in the present study.…”

Section: Discussionmentioning

confidence: 99%

Sustained cardiac programming by short‐term juvenile exercise training in male rats

Asif

Wlodek

Black

et al. 2017

The Journal of Physiology

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“…The results showed that there were no significant changes of blood lipids (Total cholesterol, LDL cholesterol, Triglyceride), renal function (serum creatinine), arterial stiffness (BaPWV) and plasma glucose (HbA1c) between non-sarcopenia and sarcopenia group, while blood lipids marker HDL cholesterol of sarcopenia group was significantly higher than that of nonsarcopenia group. We determined the expression of angiogenesis-related miRNAs (miR-20a, miR-126, miR-210, miR-221, miR-222, and miR-328) (Dews et al, 2006;Poliseno et al, 2006;Kuehbacher et al, 2007;Fasanaro et al, 2008;Soeki et al, 2016), inflammationrelated miRNAs (miR-21, miR-146a, and miR-155) (Taganov et al, 2006;Urbich et al, 2008;Wang et al, 2017) and cardiac or muscle-specific/enriched miRNAs (miR-1, miR-133a, miR-133b, miR-208b, miR-486, and miR-499) (Chen et al, 2006;Alexander et al, 2014;Soci et al, 2016). Firstly, the results of small-sample screening experiment showed that plasma miR-208b, miR-499, miR-155, miR-222, miR-328, and miR-210 levels were significantly down-regulated in sarcopenia group compared to those who non-sarcopenia.…”

Section: Subject Characteristicsmentioning

confidence: 99%

Circulating MicroRNAs in Plasma Decrease in Response to Sarcopenia in the Elderly

Zhang

et al. 2020

Front. Genet.

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sarcopenia has been defined as the aging-related disease with the declined mass, strength, and function of skeletal muscle, which is a major cause of morbidity and mortality in elders. Current diagnostic criteria of sarcopenia have not been agreed internationally, and the clinical diagnostic biomarkers for sarcopenia have not been identified. Circulating miRNAs (miRNAs, miRs) have recently been characterized as novel biomarkers for sarcopenia. However, the change of circulating miRNAs in response to sarcopenia are still not fully understood. Here, we enrolled a total of 93 elderly patients clinically diagnosed with sarcopenia and matching 93 non-sarcopenia elderly in this study. Specifically, levels of candidate circulating miRNAs which were involved in angiogenesis, inflammation and enriched in muscle and/or cardiac tissues were detected in these two groups. In small-sample screening experiments, plasma miR-155, miR-208b, miR-222, miR-210, miR-328, and miR-499 levels were significantly downregulated in sarcopenia compared to those who non-sarcopenia. In contrast, miR-1, mir-133a, miR-133b, miR-21, miR-146a, miR-126, miR-221, and miR-20a were not changed significantly. Subsequently, we expanded the sample size to further detection and verification, and found that plasma miR-155, miR-208b, miR-222, miR-210, miR-328, and miR-499 levels in the sarcopenia group were significantly reduced compared to the non-sarcoma group, which is consistent with the results of the small-sample screening experiment. In addition, we showed that ASM/Height2, handgrip strength, knee extension and 4-meter velocity in sarcopenia group were significantly lower than those in non-sarcopenia group. Here we correlated the decrease of miR-208b, miR-499, miR-155, miR-222, miR-328, and miR-210 in sarcopenia group and non-sarcopenia group with diagnostic indexes of sarcopenia (ASM/Height2, Handgrip strength and 4meter velocity) after adjusting sex. The results showed that miR-208b and miR-155 changes were significantly correlated with handgrip strength in woman, miR-208b, miR-499, and miR-222 changes were significantly correlated with ASM/Height2 in man, while other miRNAs changes did not show a strong correlation with these diagnostic indexes. In conclusion, plasma miR-208b, miR-499, miR-155, miR-222, miR-328, and miR-210

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“…Differently from which is found in pathological CH [61], high volume ET decreases the expression of cardiac miRNA-208a in healthy, induces the upregulation of targets such as THRAP-1, Purβ, and Sox6, and improves the balance between βMHC and αMHC gene expression [2,84]. In addition, in recent study, Fernandes et al [85] showed that aerobic ET prevents weight gain and pathological CH in obese Zucker rats, via increase of cardiac MED13 by regulation of miRNA-208.…”

Section: Mirnas Regulation By Exercise Training In Cardiac Remodelingmentioning

confidence: 99%

Noncoding RNAs in the Cardiovascular System: Exercise Training Effects

Pereira¹,

Gatto²,

Oliveira³

et al. 2020

Muscle Cells - Recent Advances and Future Perspectives

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Exercise training (ET) represents a non-pharmacological treatment that can attenuate or even reverse the process of cardiovascular diseases (CVD), by stimulating protein synthesis, angiogenesis, mitochondrial biogenesis, anti-inflammatory, and anti-oxidative effects that are involved to enhance the performance and improved quality of life. Despite the benefits of exercise, the intricacies of their underlying molecular mechanisms remain largely unknown. Noncoding RNAs (ncRNAs) have been recognized as a major regulatory network governing gene expression in several physiological processes and appeared as pivotal modulators in a myriad of cardiovascular processes under physiological and pathological conditions. However, little is known about ncRNA expression and role in response to exercise. Here we review the current understanding of the ncRNA role in exerciseinduced adaptations focused on the cardiovascular system and address their potential role in clinical applications for cardiovascular diseases.

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

Cited by 54 publications

References 40 publications

Sustained cardiac programming by short‐term juvenile exercise training in male rats

Sustained cardiac programming by short‐term juvenile exercise training in male rats

Circulating MicroRNAs in Plasma Decrease in Response to Sarcopenia in the Elderly

Noncoding RNAs in the Cardiovascular System: Exercise Training Effects

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