MiR-808 inhibits cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction by regulating TGF-ß1 signaling pathway.

OBJECTIVE: To investigate the effects of micro ribonucleic acid (miR)-808 on cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction (MI) by regulating the transforming growth factor-ß1 (TGF-ß1) signaling pathway. MATERIALS AND METHODS: A total of 24 specific pathogen-free female Sprague-Dawley rats were enrolled and randomly divided into normal group, model group, and miR-808 group, 8 rats in each group. In the model group and miR-808 group, MI model was prepared by ligation of the left anterior descending coronary artery in the rats. The miR-808 group was transfected with miR-808 lentivirus after the model was established. After one week of intervention, the expression of TGF-ß1 was detected by reverse transcription-polymerase chain reaction (RT-PCR). The cardiac function of rats was determined by echocardiography. The myocardium of rats was observed by Masson staining. The cardiomyocyte apoptosis of rats was examined by TdT-mediated dUTP-biotin nick end labeling (TUNEL) method. The expression levels of caspase-3 and caspase-9 were detected by Western blotting. RESULTS: The expression of TGF-ß1 mRNA was higher in the model group than that in the normal group (p<0.05), but compared with that in the model group, it was lower in the miR-808 group. The myocardial function and cardiomyocyte survival rate in the miR-808 group was better and higher than those in the model group (p<0.05). The expression levels of caspase-3 and caspase-9 in the miR-808 group were lower than those in the model group (p<0.05). CONCLUSIONS: MiR-808 can inhibit cardiomyocyte apoptosis in rats with MI by down-regulating TGF-ß1 expression and inhibiting the expressions of caspase-3 and caspase-9.

Downregulated miRNA-26a-5p induces the apoptosis of endothelial cells in coronary heart disease by inhibiting PI3K/AKT pathway.

OBJECTIVE: Multiple microRNAs (miRNAs) are abnormally expressed in endothelial cells during the occurrence of coronary artery disease (CAD). Previous researches have demonstrated that miRNA-26a-5p participates in regulating the proliferation of vascular smooth muscle cells and angiogenesis. The aim of this study was to clarify the role of miRNA-26a-5p in regulating cellular performances of endothelial cells in the progression of CAD. PATIENTS AND METHODS: In vivo CAD model was successfully established by feeding high-fat diet in 8-week-old female ApoE/LDLR-/- mice. CAD mice were administered with miRNA-26a-5p NC or miRNA-26a-5p inhibitor, respectively. Meanwhile, coronary endothelial cells were isolated from CAD mice and normal controls. Relative levels of miRNA-26a-5p, the gene of phosphate and tension homology deleted on chromosome ten (PTEN) and vascular endothelial growth factor (VEGF) in CAD patients and coronary endothelial cells isolated from CAD mice were examined. The regulatory effect of miRNA-26a-5p on atherosclerosis-related genes in primary endothelial cells and HUVECs were detected as well. Moreover, the viability and apoptosis of primary endothelial cells with miRNA-26a-5p knockdown were assessed by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Dual-luciferase reporter gene assay was conducted to identify the relationship between miRNA-26a-5p and PTEN. Furthermore, the regulatory role of miRNA-26a-5p in phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway was examined in endothelial cells. RESULTS: MiRNA-26a-5p and VEGF were significantly downregulated in CAD patients and primary endothelial cells isolated from CAD mice. However, PTEN was significantly upregulated. CAD mice administrated with miRNA-26a-5p inhibitor exhibited remarkably upregulated ET-1, TxA2, and ANG II, as well as downregulated eNOS and PGI2. Conversely, transfection of miRNA-26a-5p mimics in HUVECs obtained the opposite trends. PTEN was identified as the direct target gene of miRNA-26a-5p. Moreover, significantly reduced viability and enhanced apoptotic rate were observed in endothelial cells isolated from CAD mice administrated with miRNA-26a-5p inhibitor. In addition, the protein level of p-AKT in endothelial cells with miRNA-26a-5p knockdown was significantly down-regulated. CONCLUSIONS: MiRNA-26a-5p influences the proliferative and apoptotic abilities of endothelial cells isolated from CAD mice by targeting PTEN to activate PI3K/AKT pathway.

Temperature and boundary influence on cement hydration monitoring using embedded piezoelectric transducers.

In this study, the hydration process was monitored using embedded ultrasonic transducers. It was found that the ultrasonic amplitude decreased and fluctuated at the very early age, several hours after the beginning of fast hydration. The embedded transducers are very different from the surface coupled ones for they were directly influenced by the cement paste, such as the varying temperature and the boundary condition. Experiments were carried out to find out which factor result in such decrease and fluctuation. Test results showed that both the temperature and boundary conditions affect the ultrasonic measurement. When the hydration progressed under constant temperature, the amplitude of the ultrasonic wave decreased smoothly during certain period. When the hardened specimen was tested, it was found that the amplitude would decrease obviously with the increasing of temperature and vice versa. The findings could be used to interpret the amplitude plot obtained in the normal hydration monitoring using embedded transducers.