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CxVB3 infection and cardiac function

ABSTRACT: Male, adolescent A/J mice (4-5 week old) were either infected (IP) with coxsackievirus B3 (CVB3; 105 pfu) or PBS. CVB3 is a cardiotropic virus which leads to cardiac inflammation and fibrosis within 9 days after IP injection. We wanted to know how the virus would impact long term cardiac function, and whether changes in cardiac function could be associated with cardiac transcriptional regulation. At days 3, 9 and 30 days post-infection, hearts were imaged with 2D echocardiography (Sonos 5500, Philips). Briefly, mice were anesthesized subcutaneously with ketamine (0.45mg/kg) and xylazine (0.03mg/kg). Mice were placed in a dorsal recumbency position and the following systolic and diastolic measurements were taken (N=5 heart beats) using an S-12 (12MHz; Sonos 5000, Philips) probe: parasternal long axis, and short axis at the level of the mitral valve and papillary muscles. Measurements were utilized for calculation of wall thickness and functional parameters. Then, heart tissues were flash frozen (N=4 mice/group except CVB3 infected 30 day samples N=2) for hybridization to Affymetrix MG U74Av2 arrays. Keywords: time-course

ORGANISM(S): Mus musculus

PROVIDER: GSE1457 | GEO | 2004/12/01

SECONDARY ACCESSION(S): PRJNA90009

REPOSITORIES: GEO

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Project description:In this model of ventilator-induced lung injury (VILI), we compared the gene expression profile of whole lungs extracted from sponaneously breathing mice (control, c) or mouse submitted to 8 hours mechanical venitlation with 12 ml/kg tidal volume 2cmH2O of positive end expiratory pressure (PEEP) (ventilation, v). Spontaneously breathing NOD/shi mice were randomized to control (n=3) or ventilation (n=5) condition. In brief, mice were anesthetized with the injection of ketamine (65 mg/kg, ip), acepromazine (2 mg/kg, ip) and xylazine (13 mg/kg, ip)(Henry Schein Inc., Melville, NY). Once deep sedation was achieved, a tracheostomy was performed and a PE-10 cannula was inserted in the trachea and stabilized with silk ligature. Control animals were immediately sacrificied with a supra-physiological dose of ketamine (300 mg/kg, ip). For ventilated mice, the cannula was connected to a custom built Voltek rodent ventilator (Voltek Enterprises, Toronto, CA). We ventilated mice for 8 hours using 2cmH2O positive end expiratory pressure (PEEP), inflating the lungs every hour to 20 cmH2O pressure as we have previously described. (16). The chest muscle was paralyzed with the injection of pancurorium (1mg/kg, ip)(Sigma-Aldrich) in ventilated mice to avoid spontaneous breathing. Heart rate and respiratory rate was continuously monitored and additional anesthesia was provided if a >15% increase in these parameters was detected. The animal protocol was approved by the BWH Institutional Animal Care and Use Committee (protocol #04477). Ventilated animals At the end of the each experiment, the animals were sacrificed with a supra-physiological dose of ketamine (300 mg/kg, ip). Subsequently, the chest cavity was opened, and the right lung was isolated and ligated at the main bronchus.Lungs were harvested and snap frozen in liquid nitrogen for total RNA extraction. Total RNA was extracted from lungs of controls (n=3) and mice submitted to ventilation (n=5) and there gene expression profiles were compared.

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CxVB3 infection and cardiac function

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