Project description:A porcine microarray study of right ventricular failure due to coronary artery ligation of the right ventricular free wall and subsequent treatment of right ventricular failure by volume unloading using a shunt between superior vena cava and the pulmonary artery (Glenn-shunt) 1. Surgical preparation with a 12 mm graft between superior vena cava and pulmonary artery, the graft is then clamped - Baseline sample using a biopsy needle. 2. After surgical preparation the coronary arteries of the right ventricular free wall are ligated, then heart failure develops over 120 minutes - Failure sample using a biopsy needle. 3. The shunt is then opened and the superior vena cava closed between the shunt and right atrium, diverting the blood from superior vena cava through the shunt for a period of 15 minutes partially unloading the right ventricle - Shunt sample using a biopsy needle. A series of six pigs, three samples from each animal: baseline, failure and shunt/treatment.
Project description:Right ventricular heart failure (RVF) associated with pulmonary hypertension (PH) is characterized by a distinct gene expression pattern when compared with functional compensatory hypertrophy. Carvedilol treatment after RVF has been established reduces right ventricle (RV) hypertrophy and improves the RV function. In addition, carvedilol treatment has been shown to alter the gene expression of select genes. We sought to identify, on a genome-wide basis, the effect of carvedilol on gene expression. RVF was induced in male Sprague-Dawley rats by the combination of VEGF-receptor blockade and chronic hypoxia; thereafter, one group was treated with carvedilol. RNA was isolated from the RV and subjected to microarray analysis. A prediction analysis of the carvedilol-treated RVs showed that carvedilol treated RVs most resembled in their expression pattern the RVF pattern. However, an analysis beyond the boundaries of the prediction set revealed a small set of genes associated with carvedilol reversal of RVF. Pathway analysis of this set of genes revealed expression changes of genes involved in cardiac hypertrophy, mitochondrial dysfunction, protein ubiquitination, and sphingolipid metabolism. Genes encoding proteins in the cardiac hypertrophy and protein ubiquitination pathways were downregulated in the RV by carvedilol, while genes encoding proteins in the mitochondrial dysfunction and sphingolipid metabolism pathways were upregulated by carvedilol.
Project description:Deep sequencing of mRNA from Spalax galili and Rattus norvegicus Total RNAs were isolated from the brain of female BMRs under various oxygen concentrations (3%, 6%, 10%, 14%, and 21%) for 6 hours. We also got RNAs from the brain of rats under 6%, 10%, 14%, and 21% oxygen conditions.
Project description:Heart failure is among the leading causes of death globally. Ventricular failure progresses through a hypertrophic compensatory phase followed by failure of the ventricle function through rapid decompensation. In order to unravel right heart specific mechanisms of disease, rat animal models were established that (i) reflect the slowly progressive mode of compensation / decompensation and (ii) allow comparative analyses of left versus right heart failure in the same experimental set up. Differential gene expression analysis was performed for all three treatment groups (sham, AOB, PAB), at both time points (compensation, decompensation) and for both ventricles as well as the septum
Project description:A porcine microarray study of acute right ventricular failure due to coronary artery ligation of the right ventricular free wall. 1. Baseline sample from the free right ventricular wall. 2. Ligation of the coronary arteries on the right ventricular free wall induced right ventricular heart failure. When the pressure in the right atrium rose to >20 mmHg, heart failure samples were taken from the free right ventricular wall.
Project description:Right ventricular (RV) failure plays a critical role in any type of heart failure. However, there is no specific therapy developed for RV failure. To understand RV failure, we focused on the RV specific genes. Global gene expression analysis showed that alternative complement pathway-related genes including C3 and Cfd were significantly upregulated in right ventricle in murine heart. We generated the RV failure by right ventricle-specific pressure overload model mice, pulmonary artery constriction (PAC), which induces RV failure around 14 days. After administration of C3a receptor (C3aR) antagonist, RV function was dramatically improved PAC-induced RV dysfunction in wild type mice. To investigate the role of C3a to cardiomyocyte, C3a recombinant protein was administerd to neonatal rat ventricular myocytes (NRVMs), the results that several MAP kinesis were phosphorylated by C3a. In turn, to identify the key expressed genes as downstream of C3a in NRVMs, global gene expression analysis was performed in vitro.
Project description:The aim of this project is to use an integrated approach involving TMT labeling and LC-MS/MS to quantify the dynamic changes of the whole proteome of chondrocytes of Rattus norvegicus.
