Expression signature of miRNAs and the potential role of miR‐195‐5p in high‐glucose–treated rat cardiomyocytes

Shi, Yuanqi; Yan, Caichuan; Li, Yang; Zhang, Yuhao; Zhang, Guocui; Li, Mingzhu; Li, Baoxin; Zhao, Xin

doi:10.1002/jbt.22423

Cited by 10 publications

(15 citation statements)

References 21 publications

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“…For example, research [16] reported that it could inhibit cervical cancer cells' migration and invasion by inhibiting ARL2. Recent studies [17] have found that it plays a crucially regulatory part in myocardial injury induced by high glucose, but its mechanism of action on cardiomyocytes has not been elaborated in detail. In our study, first, we established HF rat model by ligating abdominal aorta, and then we found that it expressed low in myocardium of HF rats.…”

Section: Discussionmentioning

confidence: 99%

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

Xie

Lei

et al. 2020

Bioscience Reports

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Purpose: The present study set out to investigate the effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure (HF) and its mechanism. Methods: HF rat model and hypoxia/reoxygenation (H/R) cardiomyocyte model were established. miR-195-5p expression and transforming growth factor-β1 (TGF-β1)/signal transduction protein (Smad)3 signaling pathway in HF rats and H/R cardiomyocytes were interfered. miR-195-5p expression was tested by Rt-PCR, TGF-β1/Smad3 signaling pathway related proteins were detected by Western Blot, apoptosis of HF rat cardiomyocytes was tested by TUNEL, and apoptosis of cardiomyocytes induced by H/R was checked by flow cytometry. Results: miR-195-5p was lowly expressed in myocardium of HF rats, while TGF-β1 and Smad3 proteins were high-expressed. Up-regulating miR-195-5p expression could obviously inhibit cardiomyocyte apoptosis of HF rats, improve their cardiac function, and inhibit activation of TGF-β1/Smad3 signaling pathway. Up-regulation of miR-195-5p expression or inhibition of TGF-β1/Smad3 signaling pathway could obviously inhibit H/R-induced cardiomyocyte apoptosis. Dual-luciferase reporter enzyme verified the targeted relationship between miR-195-5p and Smad3. Conclusion: miR-195-5p can inhibit cardiomyocyte apoptosis and improve cardiac function in HF rats by regulating TGF-β1/Smad3 signaling pathway, which may be a potential target for HF therapy.

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Section: Discussionmentioning

confidence: 99%

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

Xie

Lei

et al. 2020

Bioscience Reports

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“…GDM, gestational diabetes mellitus; GH, gestational hypertension; miR, microRNA; PE, preeclampsia; PPCM, peripartum cardiomyopathy male STZ mice, while myocardial capillary density and coronary blood flow were improved [147]. Similarly, miR-195-5p expression in rat cardiomyocytes is upregulated by high glucose stimulation [148]. Here, it was shown that silencing miR-195-5p rescues high-glucoseinduced hERG potassium ion channel deficiency by restoring serum and glucocorticoid-regulated kinase 1 (SGK1) expression [148].…”

Section: Dysregulated Mirnas In Gestational Diabetes Mellitusmentioning

confidence: 99%

Pregnancy-associated cardiac dysfunction and the regulatory role of microRNAs

et al. 2020

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Many crucial cardiovascular adaptations occur in the body during pregnancy to ensure successful gestation. Maladaptation of the cardiovascular system during pregnancy can lead to complications that promote cardiac dysfunction and may lead to heart failure (HF). About 12% of pregnancy-related deaths in the USA have been attributed to HF and the detrimental effects of cardiovascular complications on the heart can be long-lasting, pre-disposing the mother to HF later in life. Indeed, cardiovascular complications such as gestational diabetes mellitus, preeclampsia, gestational hypertension, and peripartum cardiomyopathy have been shown to induce cardiac metabolic dysfunction, oxidative stress, fibrosis, apoptosis, and diastolic and systolic dysfunction in the hearts of pregnant women, all of which are hallmarks of HF. The exact etiology and cardiac pathophysiology of pregnancy-related complications is not yet fully deciphered. Furthermore, diagnosis of cardiac dysfunction in pregnancy is often made only after clinical symptoms are already present, thus necessitating the need for novel diagnostic and prognostic biomarkers. Mounting data demonstrates an altered expression of maternal circulating miRNAs during pregnancy affected by cardiovascular complications. Throughout the past decade, miRNAs have become of growing interest as modulators and biomarkers of pathophysiology, diagnosis, and prognosis in cardiac dysfunction. While the association between pregnancy-related cardiovascular complications and cardiac dysfunction or HF is becoming increasingly evident, the roles of miRNA-mediated regulation herein remain poorly understood. Therefore, this review will summarize current reports on pregnancy-related cardiovascular complications that may lead to cardiac dysfunction and HF during and after pregnancy in previously healthy women, with a focus on the pathophysiological role of miRNAs.

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“…High glucose alone can promote pathological cardiac development by accelerating hypertrophy, promoting ER stress, increasing ROS production, and ultimately leading to apoptosis (Ng et al, 2018;Zhang X. et al, 2018;Shi et al, 2019). When uncoupled from oxidative phosphorylation, glycolysis produces glycolytic intermediates that can accelerate flux through nonanapleurotic pathways, such as the pentose phosphate pathway (PPP), hexosamine biosynthetic pathway, or lactate shuttling (Gupte et al, 2006;Gibb et al, 2017).…”

Section: Glucotoxicitymentioning

confidence: 99%

“…For instance, elevation of miRNA-195 upregulates multiple genes associated with hypertrophic development. Exogenous administration of this oligonucleotide can promote hypertrophy and alter cardiac mitochondrial function, while the complementary oligonucleotide provides a protective effect (Shi et al, 2019;Wang et al, 2019). Lastly, increased use of glucose has been shown to induce cell growth (Kolwicz et al, 2013;Shao et al, 2018) and alter epigenetic regulation in the nucleus (Shao et al, 2018;Lombardi et al, 2019).…”

Section: Glucotoxicitymentioning

confidence: 99%

Changes in Myocardial Metabolism Preceding Sudden Cardiac Death

et al. 2020

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Heart disease is widely recognized as a major cause of death worldwide and is the leading cause of mortality in the United States. Centuries of research have focused on defining mechanistic alterations that drive cardiac pathogenesis, yet sudden cardiac death (SCD) remains a common unpredictable event that claims lives in every age group. The heart supplies blood to all tissues while maintaining a constant electrical and hormonal feedback communication with other parts of the body. As such, recent research has focused on understanding how myocardial electrical and structural properties are altered by cardiac metabolism and the various signaling pathways associated with it. The importance of cardiac metabolism in maintaining myocardial function, or lack thereof, is exemplified by shifts in cardiac substrate preference during normal development and various pathological conditions. For instance, a shift from fatty acid (FA) oxidation to oxygen-sparing glycolytic energy production has been reported in many types of cardiac pathologies. Compounded by an uncoupling of glycolysis and glucose oxidation this leads to accumulation of undesirable levels of intermediate metabolites. The resulting accumulation of intermediary metabolites impacts cardiac mitochondrial function and dysregulates metabolic pathways through several mechanisms, which will be reviewed here. Importantly, reversal of metabolic maladaptation has been shown to elicit positive therapeutic effects, limiting cardiac remodeling and at least partially restoring contractile efficiency. Therein, the underlying metabolic adaptations in an array of pathological conditions as well as recently discovered downstream effects of various substrate utilization provide guidance for future therapeutic targeting. Here, we will review recent data on alterations in substrate utilization in the healthy and diseased heart, metabolic pathways governing cardiac pathogenesis, mitochondrial function in the diseased myocardium, and potential metabolism-based therapeutic interventions in disease.

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Expression signature of miRNAs and the potential role of miR‐195‐5p in high‐glucose–treated rat cardiomyocytes

Cited by 10 publications

References 21 publications

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

Effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure by regulating TGF-β1/Smad3 signaling pathway

Pregnancy-associated cardiac dysfunction and the regulatory role of microRNAs

Changes in Myocardial Metabolism Preceding Sudden Cardiac Death

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