RESUMO
Background: Myocardial infarction (MI) is a serious condition, caused by acute, persistent ischemia or hypoxia of a coronary artery and responsible for heart failure and sudden death. This study aimed to investigate the effects of catechin, one of the main active components of green tea, on hypoxia-induced MI cell model, as well as the underlying possible mechanism. Methods: Cell viability, proliferation, apoptosis, and the expression of microRNA-92a (miR-92a) after hypoxia stimulation and/or catechin treatment were assessed using cell counting kit-8 (CCK-8) assay, western blotting, annexin V-FITC/PI staining and qRT-PCR, respectively. miRNA transfection was performed to change the expression of miR-92a. The effects of miR-92a on hypoxia and catechin-treated H9c2 cell viability, proliferation and apoptosis were evaluated. Finally, western blotting was conducted to measure the expression of core factors in the c-Jun N-terminal kinase (JNK) signaling pathway. Results: Hypoxia stimulation significantly inhibited H9c2 cell viability and proliferation, induced cell apoptosis and up-regulated miR-92a expression. Catechin markedly protected H9c2 cells from hypoxia-induced viability loss, proliferation inhibition, and apoptosis enhance, as well as miR-92a expression increase. Furthermore, suppression of miR-92a enhanced the protective effects of catechin on hypoxia-induced H9c2 cells. Overexpression of miR-92a had opposite effects. Catechin activated the JNK pathway in H9c2 cells by down-regulating miR-92a. Conclusion: Catechin protected H9c2 cells from hypoxia-induced injury by regulating miR-92a and JNK signaling pathway. Our findings facilitate the understanding of the protective activity of catechin in hypoxia-induced MI cell injury and provide a theoretical basis for further explore treatment of MI by using catechin.
RESUMO
BACKGROUND: The E-26 transformation-specific related gene (ERG) is frequently expressed in cytogenetically normal acute myeloid leukemia (CN-AML). Herein, we performed a meta-analysis to investigate the relationship between the prognostic significance of ERG expression and CN-AML. METHODS: A systematic review of PubMed database and other search engines were used to identify the studies between January 2005 and November 2016. A total of 667 CN-AML patients were collected from seven published studies. Of the 667 patients underwent intensive chemotherapy, 429 had low expression of ERG and 238 had high expression of ERG. Summary odds ratio (OR) and the 95% confidence interval (CI) for the ERG expression and CN-AML were calculated using fixed- or random-effects models. Heterogeneity was assessed using Chi-squared-based Q- statistic test and I2 statistics. All statistical analyses were performed using R.3.3.1 software packages (R Foundation for Statistical Computing, Vienna, Austria) and RevMan5.3 (Cochrane Collaboration, Copenhagen, Denmark). RESULTS: Overall, patients with high ERG expression had a worse relapse (OR = 2.5127, 95% CI: 1.5177-4.1601, P = 0.0003) and lower complete remission (OR = 0. 3495, 95% CI: 0.2418-0.5051, P< 0.0001). With regard to the known molecular markers, both internal tandem duplications of the fms-related tyrosine kinase 3 gene (OR = 3.8634, 95% CI: 1.8285-8.1626, P = 0.004) and brain and acute leukemia, cytoplasmic (OR = 3.1538, 95% CI: 2.0537-4.8432, P< 0.0001) were associated with the ERG expression. In addition, the results showed a statistical significance between French-American-British (FAB) classification subtype (minimally differentiated AML and AML without maturation, OR = 4.7902, 95% CI: 2.7772-8.2624, P< 0.0001; acute monocytic leukemia, OR = 0.2324, 95% CI: 0.0899-0.6006, P = 0.0026) and ERG expression. CONCLUSION: High ERG expression might be used as a strong adverse prognostic factor in CN-AML.
