Activation of mitogen-activated protein kinases in experimental cerebral ischemia
F. Lennmyr
Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden,
Department of Anaesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, Sweden,
Search for more papers by this authorS. Karlsson
Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden,
Search for more papers by this authorP. Gerwins
Department of Genetics and Pathology, Uppsala University Hospital, Uppsala, Sweden
Search for more papers by this authorK. A. Ata
Department of Genetics and Pathology, Uppsala University Hospital, Uppsala, Sweden
Search for more papers by this authorA. Terént
Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden,
Search for more papers by this authorF. Lennmyr
Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden,
Department of Anaesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, Sweden,
Search for more papers by this authorS. Karlsson
Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden,
Search for more papers by this authorP. Gerwins
Department of Genetics and Pathology, Uppsala University Hospital, Uppsala, Sweden
Search for more papers by this authorK. A. Ata
Department of Genetics and Pathology, Uppsala University Hospital, Uppsala, Sweden
Search for more papers by this authorA. Terént
Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden,
Search for more papers by this authorAbstract
Lennmyr F, Karlsson S, Gerwins P, Ata KA, Terént A. Activation of mitogen-activated protein kinases in experimental cerebral ischemia. Acta Neurol Scand 2002: 106: 333–340. © Blackwell Munksgaard 2002.
Objectives– Mitogen-activated protein kinases (MAPK) regulate cell survival and differentiation. The aim of the present study is to investigate the activation pattern of different MAPKs [extracellular signal-regulated kinase (ERK), c-jun-N-terminal kinase (JNK) and p38] after cerebral ischemia. Material and methods– Rats were subjected to cerebral ischemia using a model for transient (2 h) and permanent middle cerebral artery occlusion (MCAO). The rats were allowed 6 h to 1 week of survival before immunohistochemical evaluation with phospho-specific antibodies, recognizing activated MAPKs. Results– ERK was activated in ipsilateral blood vessels, neurons and glia, but also in contralateral vessels. JNK activation was absent in neurons but appeared in arterial blood vessels and glia at the lesion side. Active p38 was observed in macrophages in maturing infarcts. Conclusions– ERK and JNK may participate in the angiogenic response to cerebral ischemia. ERK, but not JNK, was activated in neurons, possibly indicating a pathophysiologic role. Active p38 might be involved in the inflammatory reaction.
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