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Increased atherosclerotic lesion area in apoE deficient mice overexpressing bovine growth hormone

Journal article
Authors Irene Andersson
Anna Ljungberg
L. Svensson
Li-Ming Gan
J. Oscarsson
Göran Bergström
Published in Atherosclerosis
Volume 188
Issue 2
Pages 331-40
ISSN 0021-9150 (Print)
Publication year 2006
Published at Wallenberg Laboratory
Institute of Neuroscience and Physiology, Department of Physiology
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 331-40
Language en
Keywords Animals, Aorta/*pathology, Apolipoproteins E/*deficiency/genetics, Atherosclerosis/metabolism/*pathology, Blood Pressure, C-Reactive Protein/genetics/metabolism, Crosses, Genetic, DNA Primers, *Diet, *Disease Models, Animal, Growth Hormone/genetics/*metabolism, Mice, Mice, Knockout, Serum Amyloid A Protein/metabolism
Subject categories Medical and Health Sciences


Human growth hormone (GH) excess is linked to increased cardiovascular morbidity and mortality. However, little is known about the effect of GH excess on atherosclerosis. We developed a new mouse model to assess the hypothesis that GH overexpression accelerates atherosclerotic lesion formation. apoE(-/-) mice were crossed with bovine GH (bGH) transgenic mice to yield apoE(-/-) mice overexpressing bGH (apoE(-/-)/bGH). The mice were fed either standard or Western diet. At 22 weeks, atherosclerotic lesion area of thoracic aorta was larger in apoE(-/-)/bGH mice compared with littermate apoE(-/-) mice fed either diet (standard: +161+/-50%, Western: +430+/-134%). Aortic sinus lesions were more severe in apoE(-/-)/bGH mice fed standard diet compared with littermate apoE(-/-) mice. apoE(-/-)/bGH mice had lower (VLDL+LDL)/HDL ratios compared with littermate apoE(-/-) mice, while systolic blood pressure was higher in apoE(-/-)/bGH mice, irrespective of diet. The levels of serum amyloid A and hepatic CRP mRNA were higher in apoE(-/-)/bGH mice than in littermate apoE(-/-) mice. In conclusion, this study shows that excess GH augments the development of atherosclerosis in apoE(-/-) mice. The mechanisms could be direct effects of GH on cellular processes in the vessel wall or the result of concomitant processes such as hypertension or a general inflammatory state.

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