Objective: To explore the effects of long non-coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) on the proliferation and apoptosis of hypoxic myocardial cells by regulating the expression of forkhead box O1 (FoxO1).
Materials And Methods: The myocardial A10 cell lines were divided into myocardial cell group (group A), hypoxic myocardial cell group (group B), and hypoxic myocardial cell + transfection with lncRNA MEG3 mimic group (group C). The correlations of the adenosine triphosphate (ATP) concentration, the degree of apoptosis, and the proliferation with FoxO1 and FoxO3a proteins in the cells were observed via ATP assay, Cell Counting Kit-8 (CCK-8) assay, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, Western blotting, and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR), respectively.
Results: The ATP concentration in myocardial cells was the highest in group A (p<0.05), and it was higher in group B than that in group C (p<0.05). The results of the CCK-8 assay showed that the proliferation rate of the myocardial cells was the highest in group A and the lowest in group C (p<0.05), and it was significantly increased in group B compared with that in group C (p<0.05). The results of the TUNEL assay revealed that the normal cells displayed the purple color, and apoptotic cells displayed the green color. The myocardial cells were arranged orderly, and the number of apoptotic cells was smaller in group A, the number of apoptotic cells was significantly larger in group B than that in group A, and it was the largest in group C (p<0.05). Moreover, the results of Western blotting manifested that the concentrations of FoxO1 and FoxO3 proteins in myocardial cells were the lowest in group A (p<0.05), and they were significantly higher in group C than those in group B (p<0.05). According to the results of qRT-PCR, the mRNA expressions of FoxO1 and FoxO3 in myocardial cells were the lowest in group A (p<0.05), and they were remarkably lower in group B than those in group C (p<0.05).
Conclusions: LncRNA MEG3 can increase the activity of FoxO1 to promote myocardial apoptosis in a hypoxic environment.
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http://dx.doi.org/10.26355/eurrev_201908_18665 | DOI Listing |
PLoS One
January 2025
Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.
Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.
Redox Biol
January 2025
Department of Anesthesiology, Beijing Friendship Hospital, Capital Medical University, Beijing, China; Department of Anesthesiology, Shengli Clinical Medical College of Fujian Medical University, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, Fuzhou, China. Electronic address:
Available evidence indicates that neuregulin-1 (NRG-1) can provide a protection against myocardial ischemia/reperfusion (I/R) injury and is involved in various cardioprotective interventions by potential regulation of mitophagy. However, the molecular mechanisms linking NRG-1 and mitophagy remain to be clarified. In this study, both an in vivo myocardial I/R injury model of rats and an in vitro hypoxia/reoxygenation (H/R) model of H9C2 cardiomyocytes were applied to determine whether NRG-1 postconditioning attenuated myocardial I/R injury through the regulation of mitophagy and to explore the underlying mechanisms.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of Hepatobiliary Surgery, The First People's Hospital of Zhaoqing, Zhaoqing City, Guangdong Province, People's Republic of China.
Background: Myocardial ischemia/reperfusion (I/R) injury significantly impacts the recovery of ischemic heart disease patients. Non-coding RNAs, including miRNAs, have been increasingly recognized for their roles in regulating cardiomyocyte responses to hypoxia/reoxygenation (H/R) injury. miR-181c-5p, in particular, has been implicated in inflammatory and apoptotic processes, suggesting its potential involvement in exacerbating cellular damage.
View Article and Find Full Text PDFStem Cell Rev Rep
January 2025
Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Background: The hypobaric hypoxic atmosphere can cause adverse reactions or sickness. The purpose of this study was to explore the preventive effect and mechanism of human umbilical cord mesenchymal stem cells (hUC-MSCs) on acute pathological injury in mice exposed to high-altitude.
Methods: We pretreated C57BL/6 mice with hUC-MSCs via the tail vein injection, and then the mice were subjected to hypobaric hypoxic conditions for five days.
Redox Rep
December 2025
Department of Cardiology, Fujian Medical University Union Hospital, Fuzhou, Fujian, People's Republic of China.
Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.
Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model.
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