Indole-3-Acetic Acid/Horseradish Peroxidase-Induced Apoptosis Involves Cell Surface CD95 (Fas/APO-1) Expression

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  • Kim Dong-Seok
    Research Division for Human Life Sciences, Seoul National University Department of Dermatology, Seoul National University College of Medicine
  • Kim So-Young
    Department of Dermatology, Seoul National University College of Medicine
  • Jeong Yun-Mi
    Department of Dermatology, Seoul National University College of Medicine
  • Jeon Sang-Eun
    Department of Dermatology, Seoul National University College of Medicine
  • Kim Myo-Kyoung
    Pharmacy Practice, Thomas J. Long School of Pharmacy, University of the Pacific
  • Kwon Sun-Bang
    Welskin Co., Ltd.
  • Park Kyoung-Chan
    Department of Dermatology, Seoul National University College of Medicine

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Abstract

Recently, we showed that a combination of indole-3-acetic acid (IAA) and horseradish peroxidase (HRP) produces hydrogen peroxide (H2O2), and that this leads to the apoptosis of G361 human melanoma cells. In the present study, flow cytometric analysis confirmed that H2O2 is involved the IAA/HRP-induced apoptotic process. We also found that IAA/HRP increases cell surface CD95 (Fas/APO-1) expression, and that this is blocked by catalase treatment. Furthermore, blocking CD95 with a neutralizing antibody significantly restored IAA/HRP-induced apoptosis. In addition, the IAA/HRP-induced activations of CD95 downstream molecules, i.e., caspase-8, Bid, and caspase-3, were also inhibited by catalase. Moreover, a caspase-8 inhibitor significantly blocked IAA/HRP-induced apoptosis. These results indicate that IAA/HRP-induced apoptosis involves a CD95-initiated death receptor signaling pathway initiated by hydrogen peroxide.

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