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J. Biochem, 2004, Vol. 135, No. 3 439-446
© 2004 The Japanese Biochemical Society

BIOCHEMISTRY

Nerve Growth Factor Attenuates Endoplasmic Reticulum Stress-Mediated Apoptosis via Suppression of Caspase-12 Activity

Koji Shimoke*,1, Hisayuki Amano1, Soichiro Kishi1, Hitoshi Uchida1, Motoshige Kudo2 and Toshihiko Ikeuchi1

1 Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University, 3-3-35 Yamate-cho, Suita, Osaka 564-8680; and 2 Second Department of Pathology, Tokyo Medical University, 6-7-1 Nishi-Shinjuku, Shinjuku-ku, Tokyo 160-0023

Following endoplasmic reticulum (ER) stress, which occurs via inhibition of the glycosylation of newly synthesized proteins, caspase family proteins are activated to promote ER stress-mediated apoptosis. Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity. Detailed analysis of the mechanism underlying the NGF-mediated cell survival revealed that the activities of all seriate caspases were reduced through the phosphatidylinositol 3-kinase (PI3-K) signaling pathway induced by NGF. Moreover, we found that the activity of c-Jun N-terminal kinase (JNK) was not essential for the tunicamycin-induced apoptosis of PC12 cells. These results demonstrate that the inactivation of caspase-12 via the NGF-mediated PI3-K signaling pathway leads to inactivation of the caspase cascade including caspase-3 and -9.

* To whom correspondence should be addressed. Tel: +81-6-6368-0853, Fax: +81-6-6330-3770, E-mail: shimoke{at}ipcku.kansai-u.ac.jp


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