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

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  • Shimoke Koji
    Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
  • Amano Hisayuki
    Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
  • Kishi Soichiro
    Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
  • Uchida Hitoshi
    Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
  • Kudo Motoshige
    Second Department of Pathology, Tokyo Medical University
  • Ikeuchi Toshihiko
    Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University

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  • Nerve Growth Factor Attenuates Endoplasmic Reticulum Stress-Mediated Apoptosis <i>via</i> Suppression of Caspase-12 Activity

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Following endoplasmic reticulum (ER) stress, which occurs via inhibition of the glyc-osylation 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 PC 12 cells. These results demonstrate that the inactivation of caspase-12 via the NGFmediated PI3-K signaling pathway leads to inactivation of the caspase cascade including caspase-3 and -9.

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