Jianzhong Wang1, Qilong Feng2, Dongke Liang3, Junfeng Shi4. 1. Intersive Care Unit, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi 030024, China. 2. Departments of Physiology, Shanxi Medical University, Taiyuan, Shanxi 030001, China. 3. Department of Anesthesiology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China. 4. Cardiovascular Medicine Department, XD Group Hospital, Xi'an, Shaanxi 710077, China. Electronic address: shijunfeng3580@163.com.
Abstract
INTRODUCTION: Acute myocardial infarction (MI) is a common cause of the morbidity and mortality of cardiovascular diseases in the world. Acute MI lead to cardiovascular output after formation of myocardial ischemia and circulatory arrest in coronary heart diseases. However, the mechanisms underlying MI injury are poorly understood. We explored the part played by miR-26a in myocardial infarction (MI). MATERIAL AND METHODS: Decreased miR-26a expression in H2O2-treated newborn murine ventricular cardiomyocytes (NMVCs) was observed, as well as in the infarcted heart of MI mouse model, compared to untreated NMVCs and healthy mouse heart tissue, respectively. Conversely, the upregulation of phosphatase and tensin homolog (PTEN) was observed in H2O2-treated NMVCs, and in infarcted hearts. An MTT assay and BrdU staining showed that H2O2 treatment attenuated cell viability in NMVCs, whereas miR-26a overexpression increased cell viability. Both TUNEL assay and flow cytometry (FC) displayed that miR-26a expression suppressed H2O2-induced cell apoptosis. Besides, miR-26a overexpression suppressed the upregulation of PTEN expression in H2O2-treated NMVCs by directly binding to PTEN 3'-UTR. RESULTS: PI3K/Akt and JAK/STAT signal transduction pathways were found to be regulated through cross-talk between miR-26a and PTEN. Furthermore, agomiR-26a treatment in MI mouse model considerably suppressed the size of the infarcted regions, and improved cardiac activity. CONCLUSIONS: MiR-26a expression in MI cardiac tissues was downregulated in response to H2O2 stress, whereas it could still protect against cell death by modulation of the PI3K/Akt and JAK/STAT signal transduction pathways by directly targeting PTEN.
INTRODUCTION: Acute myocardial infarction (MI) is a common cause of the morbidity and mortality of cardiovascular diseases in the world. Acute MI lead to cardiovascular output after formation of myocardial ischemia and circulatory arrest in coronary heart diseases. However, the mechanisms underlying MI injury are poorly understood. We explored the part played by miR-26a in myocardial infarction (MI). MATERIAL AND METHODS: Decreased miR-26a expression in H2O2-treated newborn murine ventricular cardiomyocytes (NMVCs) was observed, as well as in the infarcted heart of MI mouse model, compared to untreated NMVCs and healthy mouse heart tissue, respectively. Conversely, the upregulation of phosphatase and tensin homolog (PTEN) was observed in H2O2-treated NMVCs, and in infarcted hearts. An MTT assay and BrdU staining showed that H2O2 treatment attenuated cell viability in NMVCs, whereas miR-26a overexpression increased cell viability. Both TUNEL assay and flow cytometry (FC) displayed that miR-26a expression suppressed H2O2-induced cell apoptosis. Besides, miR-26a overexpression suppressed the upregulation of PTEN expression in H2O2-treated NMVCs by directly binding to PTEN 3'-UTR. RESULTS: PI3K/Akt and JAK/STAT signal transduction pathways were found to be regulated through cross-talk between miR-26a and PTEN. Furthermore, agomiR-26a treatment in MI mouse model considerably suppressed the size of the infarcted regions, and improved cardiac activity. CONCLUSIONS: MiR-26a expression in MI cardiac tissues was downregulated in response to H2O2 stress, whereas it could still protect against cell death by modulation of the PI3K/Akt and JAK/STAT signal transduction pathways by directly targeting PTEN.
Authors: Nesrine Ebrahim; Hajir A Al Saihati; Ola Mostafa; Amira Hassouna; Sameh Abdulsamea; Eman Abd El Aziz M El Gebaly; Nashwa Hassan Abo-Rayah; Dina Sabry; Mohamed El-Sherbiny; Abdelmonem G Madboly; Noha Ibrahim Hussien; Raja El Hasnaoui Saadani; Hasnaa Ali Ebrahim; Omnia A M Badr; Nehal M Elsherbiny; Rabab F Salim Journal: Int J Mol Sci Date: 2022-05-25 Impact factor: 6.208