alexa Social disruption stress increases IL-6 levels and accelerates atherosclerosis in ApoE- - mice.
Clinical Sciences

Clinical Sciences

Cardiovascular Pharmacology: Open Access

Author(s): Bernberg E, Ulleryd MA, Johansson ME, Bergstrm GM, Bernberg E, Ulleryd MA, Johansson ME, Bergstrm GM

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Abstract INTRODUCTION: We have previously shown that different forms of stress have distinctive effects on atherogenesis in mice. We showed that social stress increase atherosclerosis in ApoE(-/-) mice, while more physical forms of stress do not. Here we evaluated the effect of social disruption (SDR) stress on atherogenesis and evaluated cytokine release after SDR-stress and five more physical stressors. METHODS: Male ApoE(-/-) mice were exposed to SDR-stress during 12 weeks, and atherosclerotic plaque area was assessed in aorta, aortic root and innominate artery. Further, male C57BL/6 mice were exposed to SDR-stress or five physical stressors, and cytokine and corticosterone levels were analyzed in plasma/serum samples immediately after stress. RESULTS: We found a correlation between the level of SDR-stress and atherosclerotic plaque area in aorta and a numerical increased plaque area in aortic root. SDR stress did not affect histological features of plaque composition. However, SDR-stress increased levels of corticosterone, IL-6 and CXCL1. Plasma corticosterone increased for all five physical stressors, but IL-6 and CXCL1 only increased in the group exposed to restraint combined with rat odor. CONCLUSIONS: These findings suggest that SDR-stress is indeed atherogenic, in contrast to our previous results using the physical stressors. A possible explanation to this difference is that SDR-stress, but not physical stressors, leads to release of the pro-inflammatory cytokines IL-6 and CXCL1. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved. This article was published in Atherosclerosis and referenced in Cardiovascular Pharmacology: Open Access

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