a-doxorubicin-induced-murine-model-of-dilated-cardiomyopathy-in-vivo

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Dilated cardiomyopathy (DCM) refers to a spectrum of heterogeneous myocardial disorders characterized by ventricular dilation and depressed cardiac ...

Clinical College of Nanjing Medical University

Hepatocellular carcinoma (HCC) ranks the third major cause of cancer-associated mortality globally. Numerous studies have attempted to elucidate the underlying mechanisms of HCC using various biomarkers. In the present study, two expression profiles datasets from Gene Expression Omnibus (GSE76427 and GSE84402) and data associated with liver cancer samples from The Cancer Genome Atlas (TCGA) were downloaded for integrated analysis. Five differentially expressed genes (DEGs) exhibiting high expression, including ubiquitin-conjugating enzyme 2C (UBE2C), topoisomerase II α, pituitary tumor transforming gene 1, glypican-3 and polycomb-repressive complex 1, were selected and considered as candidate genes. Enrichment analysis demonstrated that these genes were associated with Gene Ontology terms of cellular components and molecular functions, including regulation of apoptosis, stabilization of p53 and Anaphase Promoting Complex/Cyclosome (APC/C) (APC/C:Cdc20)-mediated degradation of Securin. The expression profiles of these genes in HCC, other human malignancies and different human HCC cell lines were validated using GSE14520, GSE3500 and TCGA data. The results confirmed the upregulation of UBE2C in tissues from patients with HCC or other human malignancies and human liver cancer cell lines, compared with the expression levels in the corresponding adjacent non-tumor tissues and cell lines, respectively. Patients with HCC who exhibited an increased messenger RNA level of UBE2C exhibited a significantly shorter survival time. The results of the present study suggest that the overexpression of UBE2C may be used as a novel prognostic biomarker of HCC.

Identification of the potential therapeutic target gene UBE2C in human hepatocellular carcinoma: An investigation based on GEO and TCGA databases.

The inflammation modulation effects of mesenchymal stromal cell-derived exosomes (MSC-EXO) are well established. We aimed to explore the mechanism behind the inflammatory responses of numerous exosomal cargo molecules that have been neglected in molecular biology research, and to develop an exosomal cargo delivery system that can exert a stronger therapeutic effect on myocardial ischemia-reperfusion (I/R) injury.

miRNA-181a over-expression in mesenchymal stem cell-derived exosomes influenced inflammatory response after myocardial ischemia-reperfusion injury.

Previous studies showed that miR-124 had a protective role by reducing oxidant stress and preventing cell apoptosis and autophagy. However, its role in doxorubicin-induced cardiomyopathy was less known. In our study, we confirmed increased ROS and decreased expression of miR-124 in doxorubicin-treated heart tissues and primary cardiomyocytes. The oxidative stress and cell apoptosis were alleviated by overexpressing miR-124, characterized by decreased activity of MDA and increased activity of SOD. While inhibiting miR-124 generated opposed effects. Mechanistically, our bioinformatic prediction and luciferase assay confirmed that miR-124 inhibited the expression of p66Shc, a proapoptotic signaling pathway. Our results suggested that miR-124 was hopeful to become a therapeutic target in doxorubicin-related cardiomyopathy.

MiR-124 attenuates doxorubicin-induced cardiac injury via inhibiting p66Shc-mediated oxidative stress.

Neutrophil-to-lymphocyte ratio (NLR) has been reported to serve as a prognostic marker in inflammatory diseases. The purpose of this study was to evaluate the association of NLR at admission with in-hospital mortality in patients with sepsis presenting to emergency department.This was a secondary analysis based on a single-center, retrospective, cohort study. Patients with sepsis admitted to an academic emergency department between January 2010 and January 2015 were enrolled. NLR of patients was analyzed from the hospital's electronic health record (EHR) system. A total of 174 adult patients, of which 80 (46.0%) died in hospital. The primary outcome was in-hospital mortality. Secondary outcome was 28-day mortality.Contrary to previous studies, a larger NLR was found to have less odds of in-hospital mortality, as well as the presence of bacteremia. Patients who has severe/shock or had a history of chronic heart failure (CHF) had larger odds of death during hospital. Multivariate logistic regression analysis indicated that low NLR was an independent predictor of in-hospital mortality (OR = -0.98; 95% CI -0.96 to -0.99; P = .022). However, no correlation was found between the NLR and 28-day hospital mortality in patients with sepsis (P = .988). As a predictor of in-hospital survival, the area under curve (AUC) of the NLR was 0.622 (95%CI 0.54-0.71; P = .006) and the cut-off value was 9.11 with 0.551 sensitivity and 0.707 specificity.NLR at admission was an independent predictor of in-hospital mortality of sepsis patients.

Neutrophil to lymphocyte ratio (NLR) as a prognostic marker for in-hospital mortality of patients with sepsis: A secondary analysis based on a single-center, retrospective, cohort study.

Identification of key genes and pathways in abdominal aortic aneurysm by integrated bioinformatics analysis.

This study determined whether the effect of combination therapy for hepatic carcinoma (HCC) is comparable to surgical resection (SR). According to the guidelines of the American Association for the Study of Liver Disease, radiofrequency ablation (RFA) and SR are recommended for early HCC. However, patients treated with RFA had worse long-term survival than those who received SR. Many studies utilizing the combination therapy with RFA and transarterial chemoembolization (TACE) have reported better prognosis as compared to RFA alone.

A comparison between radiofrequency ablation combined with transarterial chemoembolization and surgical resection in hepatic carcinoma: A meta-analysis.

The cardiotoxicity of isoniazid on zebrafish embryos and its underlying mechanism is unclear.

Isoniazid causes heart looping disorder in zebrafish embryos by the induction of oxidative stress.

The cardiac repair after myocardial infarction (MI) involves two phases, namely, inflammatory response and proliferative response. The former is an inflammatory reaction, evoked by different kinds of pro-inflammatory leukocytes and molecules stimulated by myocardial necrosis, while the latter is a repair process, predominated by a magnitude of anti-inflammatory cells and cytokines, as well as fibroblasts. Cardiac remodeling post-MI is dependent on the balance of individualized intensity of the post-MI inflammation and subsequent cardiac fibrosis. During the past 30 years, enormous studies have focused on investigating immune cells and mediators involved in cardiac inflammation and fibrosis, which are two interacting processes of post-MI cardiac repair. These results contribute to revealing the mechanism of adverse cardiac remodeling after MI and alleviating the impairment of cardiac function. In this study, we will broadly discuss the role of immune cell subpopulation and the involved cytokines and chemokines during cardiac repair post-MI, particular in cardiac inflammation and fibrosis.

Yihai Liu

Department of Cardiology,
Nanjing Drum Tower Hospital,
Department of Cardiology, Nanjing Drum Tower Hospital

Clinical College of Nanjing Medical University

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Yihai Liu

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Cardiology,Nanjing Drum Tower Hospital,Department of Cardiology, Nanjing Drum Tower Hospital

Clinical College of Nanjing Medical University

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Department of Cardiology,
Nanjing Drum Tower Hospital,
Department of Cardiology, Nanjing Drum Tower Hospital