Post-ischaemic silencing of p66 reduces ischaemia/reperfusion brain injury and its expression correlates to clinical outcome in stroke
نویسندگان
چکیده
Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, Schlieren CH-8952, Switzerland; Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland; Institute for Biomedical Engineering, Swiss Federal Institute of Technology Zurich (ETHZ), Zurich, Switzerland; Department of Neurology, San Raffaele Scientific Institute, Milan, Italy; Division of Psychiatry Research, University of Zurich, Schlieren, Switzerland; Department of Cardiology, Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany; Institute of Physiology, University of Zurich, Zurich, Switzerland; Institute of Veterinary Physiology, University of Zurich, Zurich, Switzerland; Department of Internal Medicine, Cantonal Hospital of Baden, Baden, Switzerland; and Cardiology, University Heart Center, University Hospital, Zurich, Switzerland
منابع مشابه
Post-ischaemic silencing of p66Shc reduces ischaemia/reperfusion brain injury and its expression correlates to clinical outcome in stroke.
AIM Constitutive genetic deletion of the adaptor protein p66(Shc) was shown to protect from ischaemia/reperfusion injury. Here, we aimed at understanding the molecular mechanisms underlying this effect in stroke and studied p66(Shc) gene regulation in human ischaemic stroke. METHODS AND RESULTS Ischaemia/reperfusion brain injury was induced by performing a transient middle cerebral artery occ...
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AIMS Stroke is a leading cause of morbidity and mortality, and its incidence increases with age. Both in animals and in humans, oxidative stress appears to play an important role in ischaemic stroke, with or without reperfusion. The adaptor protein p66(Shc) is a key regulator of reactive oxygen species (ROS) production and a mediator of ischaemia/reperfusion damage in ex vivo hearts. Hence, we ...
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