Reduced postischemic apoptosis in the hippocampus of mice deficient in interleukin-1

• Published in: Journal of comparative neurology (1911) Vol. 448; no. 2; pp. 203 - 216
• Main Authors: Mizushima, Hidekatsu, Zhou, Cheng J.i., Dohi, Kenji, Horai, Reiko, Asano, Masahide, Iwakura, Yoichiro, Hirabayashi, Takahiro, Arata, Satoru, Nakajo, Shigeo, Takaki, Atsushi, Ohtaki, Hirokazu, Shioda, Seiji
• Format: Journal Article
• Language: English
• Published: New York Wiley Subscription Services, Inc., A Wiley Company 24.06.2002
• Subjects: Animals; Apoptosis - genetics; Brain Ischemia - genetics; Brain Ischemia - metabolism; Brain Ischemia - physiopathology; Caspase 3; Caspases - metabolism; Female; global ischemia; Hippocampus - metabolism; Hippocampus - pathology; Hippocampus - physiopathology; Immunohistochemistry; Interleukin-1 - deficiency; Interleukin-1 - genetics; Interleukin-1 - metabolism; JNK Mitogen-Activated Protein Kinases; knockout mice; Male; MAP Kinase Signaling System - genetics; Mice; Mice, Knockout; Microscopy, Electron; mitogen-activated protein kinase; Mitogen-Activated Protein Kinases - metabolism; neurodegeneration; Neurons - metabolism; Neurons - pathology; Neurons - ultrastructure; nitric oxide; Nitric Oxide - biosynthesis; Nitric Oxide Synthase - metabolism; p38 Mitogen-Activated Protein Kinases; RNA, Messenger - metabolism

The cytokine interleukin‐1 (IL‐1) has been implicated in ischemic brain damage, because the IL‐1 receptor antagonist markedly inhibits experimentally induced neuronal loss. However, to date, no studies have demonstrated the involvement of endogenous IL‐1α and IL‐ 1β in neurodegeneration. We report h...