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Overexpression of apolipoprotein B attenuates pathologic cardiac remodeling and hypertrophy in response to catecholamines and after myocardial infarction in mice.

Journal article
Authors Truls Råmunddal
Malin Lindbom
Margareta Scharin Täng
Yangzhen Shao
Jan Borén
Elmir Omerovic
Published in Scandinavian Journal of Clinical & Laboratory Investigation
Volume 72
Issue 3
Pages 230-236
ISSN 0036-5513
Publication year 2012
Published at Wallenberg Laboratory
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 230-236
Language en
Links dx.doi.org/10.3109/00365513.2012.65...
Keywords Hypertrophy, apolipoprotein B, myocardial infarction, cardiac remodeling, lipids
Subject categories Cardiovascular medicine

Abstract

Abstract Introduction. The heart produces apolipoprotein (apo) B-containing lipoproteins which enables cardiac export of potentially cardiotoxic lipids. We hypothesized that overexpression of apoB attenuates the pathologic cardiac remodeling and hypertrophic response following pathological stimuli such as chronic adrenergic overstimulation and myocardial infarction (MI). Methods. Cardiac hypertrophy was induced by a chronic infusion of isoproterenol (ISO) 15 mg/kg/day for 3 weeks in human apoB transgenic mice (n9) and in non-transgenic wild-type mice (n10). As controls, apoB transgenic (N10) and wild-type mice (N10) saline infusions were used. Transthoracic echocardiography was performed at baseline and after 3 weeks of treatment to evaluate left ventricular (LV) function and morphology. To investigate the effects of expression on postinfarct hypertrophic response we induced MI in apoB transgenic mice (n8) and in wild-type controls (n11). The hearts were explanted and weighed 6 weeks post MI. Results. At baseline, WT mice had higher BW and LV mass (LVM) compared to the apoB mice. The increase in LV mass and dimensions after 3 weeks of treatment with ISO was significantly lower while systolic function was signifi cantly better in the apoB group. Six weeks post MI the apoB mice had significantly lower heart weight and heart weight to body weight ratio. The infarct size was similar in both groups. Conclusion. Overexpression of apoB attenuates the pathologic remodeling and hypertrophic response to chronic adrenergic stimulation and MI. Our results indicate that cardiac expression of apoB-containing lipoproteins might be an important regulator of myocardial structure and function.

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