Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats

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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“…HF rat model [10] was prepared by abdominal aortic stenosis method. HF was induced by ligating abdominal aorta to create a cardiac load pot.…”

Section: Establishment Of Animal Modelmentioning

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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“…Eight weeks of running on a treadmill increased the weight of the left ventricle in rats in a prior study (22). Another study showed that six weeks of resistance training increased the weight of the rat's heart (23).…”

Section: Discussionmentioning

confidence: 90%

Effect of Eight Weeks of Resistance Training with Spirulina Platensis Ingestion on the Heart Weight and Cardiac C/EBPβ Expression in Male Rats

Ahmadi

Zadeh

Habibi

et al. 2019

Middle East J Rehabil Health Stud

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Background: Resistance training and Spirulina consumption could change the expression of the gene involved in hypertrophy. Objectives: The study investigated the effect of eight weeks of resistance training with Spirulina platensis ingestion on the heart weight and cardiac CCAAT-enhancer-binding proteins beta (C/EBPβ) expression in male rats. Methods: We divided 32 male Sprague Dally rats into four groups: control (CO; n = 8), Spirulina platensis (SP; n = 8), resistance training (RE; n = 8), and Spirulina plus resistance training (SP + RE; n = 8). The resistance training group practiced five sessions a week for eight weeks. Spirulina 200 mg/kg/day was used in the supplement group and the exercise plus Spirulina platensis group. Twenty-four hours after the last training session, the gene expression was measured using real-time PCR. Results: The results showed that resistance training significantly increased heart weight (P = 0.001) and left ventricular weight (P = 0.001) but significantly decreased CEBP (P = 0.001). Spirulina insignificantly increased heart weight (P = 0.46), significantly increased left ventricular weight (P = 0.001), and significantly decreased CEBP (P = 0.02). On the other hand, resistance training plus Spirulina significantly increased heart weight (P = 0.001) and left ventricular weight (P = 0.001) but had no significant effect on C/EBPβ reduction (P = 0.10). Conclusions: A combination of resistance training and Spirulina supplementation cannot have a significant effect on the important signaling factor in heart hypertrophy.

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“…Phosphorylated MAPKs subsequently activate downstream substrates involved in cardiac hypertrophy, including c-Jun, activated transcription factor 2 and cardiomyocyte enhancer factor 2, and then regulate cellular gene transcription and protein synthesis, leading to cardiomyocyte enlargement and fibroblast proliferation in cardiac tissues (40,41). Although the role of p38 in cardiac hypertrophy remains largely elusive and controversial (42,43), ERK signaling is generally accepted to have a role in this pathology. The ERK1/2 cascade was observed in hypertrophic and failing mammalian hearts, while deletion of ERK (ERK1 −/− and ERK2 +/− ) did not cause any obvious reduction in the hypertrophic response to various stimuli (44,45).…”

Section: Discussionmentioning

confidence: 99%

HMGB1 enhances mechanical stress-induced cardiomyocyte hypertrophy in�vitro via the RAGE/ERK1/2 signaling pathway

et al. 2019

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Pressure overload-induced cardiac hypertrophy is associated with a complex spectrum of pathophysiological mechanisms, including the inflammation response. High mobility group box-1 (HMGB1), a pro-inflammatory cytokine, is not only increased in myocardium under pressure overload, but also exacerbates pressure overload-induced cardiac hypertrophy and dysfunction; however, the underlying mechanisms have remained elusive. In the present study, cultured cardiomyocytes were stimulated by mechanical stress and/or HMGB1 for various durations to examine the role of HMGB1 in cardiomyocyte hypertrophy, and to detect the expression of receptor for advanced glycation end products (RAGE), toll-like receptor 4 (TLR-4) and the activation status of mitogen-activated protein kinases (MAPKs) and Janus kinase 2 (JAK2)/STAT3. The results indicated that HMGB1 aggravated mechanical stress-induced cardiomyocyte hypertrophy. Furthermore, mechanical stress and HMGB1 stimulation activated extracellular signal-regulated kinase 1/2 (ERK1/2), P38 and JAK2/STAT3 signaling in cardiomyocytes, but an additive effect of the combined stimuli was only observed on the activation of ERK1/2. In addition, mechanical stress caused a prompt upregulation of the expression of RAGE and TLR-4 in cardiomyocytes, while the activation of ERK1/2 by HMGB1 was inhibited by blockage of RAGE, but not by blockage of TLR-4. In summary, the present results indicated that extracellular HMGB1 enhanced mechanical stress-induced cardiomyocyte hypertrophy in vitro , at least partially via the RAGE/ERK1/2 signaling pathway.

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Exercise during transition from compensated left ventricular hypertrophy to heart failure in aortic stenosis rats

Cited by 27 publications

References 60 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

Effect of Eight Weeks of Resistance Training with Spirulina Platensis Ingestion on the Heart Weight and Cardiac C/EBPβ Expression in Male Rats

HMGB1 enhances mechanical stress-induced cardiomyocyte hypertrophy in�vitro via the RAGE/ERK1/2 signaling pathway

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