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European Journal of Neuroscience 2006-Mar

Diacylglycerol kinase zeta is involved in the process of cerebral infarction.

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Tomoyuki Nakano
Yasukazu Hozumi
Hasmat Ali
Sachiko Saino-Saito
Hideyuki Kamii
Shinya Sato
Takamasa Kayama
Masahiko Watanabe
Hisatake Kondo
Kaoru Goto

Nøkkelord

Abstrakt

Diacylglycerol kinase (DGK) is an enzyme that phosphorylates a second messenger diacylglycerol (DG) and is involved in a variety of pathophysiological cellular responses. We have previously reported that DGKzeta may be involved in the selective vulnerability of hippocampal CA1 neurons in transient forebrain ischemia. In this study we aimed to further elucidate functional implications of DGK isozymes in the cerebral cortex suffering from infarction using a focal ischemic model. In the early phase of 90 min of middle cerebral artery occlusion, DGKzeta-immunoreactivity is reduced rapidly in the nucleus of cortical neurons in the ischemic core, while DGKiota and other neuronal proteins such as MAP-2 and NeuN remain intact. This suggests that rapid disappearance of DGKzeta in ischemic neurons is a quite early event precedent to neuronal degeneration in response to ischemia. Furthermore, in the late inflammatory phase of infarction DGKzeta-immunoreactivity is detected in non-neuronal cells including factor VIII-positive endothelial cells and ED-1-positive phagocytic cells. The present study suggests that DGKzeta may play roles in various processes of ischemic brain damage including neuronal death and non-neuronal inflammatory response.

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