Involvement of caspase-4 in endoplasmic reticulum stress-induced apoptosis and Aβ-induced cell death

Journal of Cell Biology - Tập 165 Số 3 - Trang 347-356 - 2004
Junichi Hitomi1,2, Taiichi Katayama1,2, Yutaka Eguchi3,2,4, Takashi Kudo5, Manabu Taniguchi1,2, Yoshihisa Koyama1,2, Takayuki Manabe1,2, Satoru Yamagishi1,2, Yoshio Bandô6, Kazunori Imaizumi7, Yoshihide Tsujimoto3,2,4, Masaya Tohyama1,2
11Department of Anatomy and Neuroscience, Department of Post-Genomics and Diseases, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan
2621st Century COE Program, Japan Society for the Promotion of Science, Chiyoda-ku, Tokyo 102-8471, Japan
32Division of Molecular Genetics, Department of Post-Genomics and Diseases, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan
47Solution Oriented Research for Science and Technology of Japan, Science and Technology Agency, Honcho 4-1-8, Kawaguchi, Saitama, 332-0012, Japan
53Division of Psychiatry and Behavioural Proteomics, Department of Post-Genomics and Diseases, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan
64Department of Anatomy, Asahikawa Medical College, Midorigaoka Higashi, Asahikawa, Hokkaido, 078-8510, Japan
75Division of Structural Cell Biology, Nara Institute of Science and Technology, Takayama, Ikoma, Nara 630-0101, Japan

Tóm tắt

Recent studies have suggested that neuronal death in Alzheimer's disease or ischemia could arise from dysfunction of the endoplasmic reticulum (ER). Although caspase-12 has been implicated in ER stress-induced apoptosis and amyloid-β (Aβ)–induced apoptosis in rodents, it is controversial whether similar mechanisms operate in humans. We found that human caspase-4, a member of caspase-1 subfamily that includes caspase-12, is localized to the ER membrane, and is cleaved when cells are treated with ER stress-inducing reagents, but not with other apoptotic reagents. Cleavage of caspase-4 is not affected by overexpression of Bcl-2, which prevents signal transduction on the mitochondria, suggesting that caspase-4 is primarily activated in ER stress-induced apoptosis. Furthermore, a reduction of caspase-4 expression by small interfering RNA decreases ER stress-induced apoptosis in some cell lines, but not other ER stress-independent apoptosis. Caspase-4 is also cleaved by administration of Aβ, and Aβ-induced apoptosis is reduced by small interfering RNAs to caspase-4. Thus, caspase-4 can function as an ER stress-specific caspase in humans, and may be involved in pathogenesis of Alzheimer's disease.

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Journal of Cell Biology

Tập 165 Số 3

347-356

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