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Cyclosporin A prevents calpain activation despite increased intracellular calcium concentrations, as well as translocation of apoptosis-inducing factor, cytochrome c and caspase-3 activation in neurons exposed to transient hypoglycemia. (2003)

Abstract
Journal Neurochemistry doi Cyclosporin prevents calpain activation despite increased intracellular calcium concentrations well translocation apoptosis inducing factor cytochrome and caspase activation neurons exposed transient hypoglycemia Michel Ferrand Drake Changlian Zhu Gunilla Gido Anker Hansen Jan Olof Karlsson Ben Bahr Naoufal Zamzami Guido Kroemer Pak Chan Tadeusz Wieloch and Klas Blomgren Laboratory for Experimental Brain Research Wallenberg Neuroscience Center Lund University Hospital Lund Sweden Department Neurosurgery Department Neurology and Neurological Sciences and Program Neurosciences Stanford University School Medicine Stanford California USA Department Pediatrics The Third Affiliated Hospital Zhengzhou University Zhengzhou China Department Pharmacology Novo Nordisk Maaloev Denmark Institute Anatomy and Cell Biology Goteborg University Goteborg Sweden Department Pharmaceutical Sciences and the Neurosciences Program University Connecticut Storrs Connecticut USA Institut Gustave Roussy Villejuif France Perinatal Center Department Physiology Goteborg University Goteborg Sweden Perinatal Center Department Pediatrics Goteborg University The Queen Silvia Children Hospital Goteborg Sweden Abstract Blockade mitochondrial permeability transition protects against hypoglycemic brain damage study the mechanisms downstream from mitochondria that may cause neuronal death investigated the effects cyclosporin subcellular localization apoptosis inducing factor and cytochrome

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Download http://lu-research.lub.lu.se/php/gateway.php?who=lr&method=getfile&file=archive/00013222/
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Repository lu:research (Sweden)
Keywords Medicine (General)
Type Journal article

Cited publications (5)
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Endogenous inhibitor for calcium-dependent cysteine protease contains four internal repeats that could be responsible for its multiple reactive sites.
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A heart mitochondrial Ca2(+)-dependent pore of possible relevance to re-perfusion-induced injury. Evidence that ADP facilitates pore interconversion between the closed and open states.
Inhibition by cyclosporin A of a Ca2+-dependent pore in heart mitochondria activated by inorganic phosphate and oxidative stress.