Oxidative Stress-induced Interaction between Autophagy and Cellular Senescence in Human Keratinocytes

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  • Yamaguchi Masahiro
    Section of Geriatric Dentistry, Department of General Dentistry, Fukuoka Dental College Research Center for Regenerative Medicine, Fukuoka Dental College
  • Kajiya Hiroshi
    Research Center for Regenerative Medicine, Fukuoka Dental College Section of Cellular Physiology, Department of Physiological Science and Molecular Biology, Fukuoka Dental College
  • Egashira Rui
    Section of Geriatric Dentistry, Department of General Dentistry, Fukuoka Dental College Research Center for Regenerative Medicine, Fukuoka Dental College
  • Yasunaga Madoka
    Research Center for Regenerative Medicine, Fukuoka Dental College Section of Orthodontics, Department of Oral Growth and Development, Fukuoka Dental College
  • Hagio-Izaki Kanako
    Research Center for Regenerative Medicine, Fukuoka Dental College Section of General Dentistry, Department of General Dentistry, Fukuoka Dental College
  • Sato Ayako
    Research Center for Regenerative Medicine, Fukuoka Dental College Section of Oral Implantology, Department of Oral Rehabilitation, Fukuoka Dental College
  • Toshimitsu Takuya
    Research Center for Regenerative Medicine, Fukuoka Dental College Dentistry for the Disabled, Department of Oral Growth and Development, Fukuoka Dental College
  • Naito Toru
    Section of Geriatric Dentistry, Department of General Dentistry, Fukuoka Dental College
  • Ohno Jun
    Research Center for Regenerative Medicine, Fukuoka Dental College

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<p>Oxidative stress in keratinocytes induces cytoprotective events, such as autophagy and cellular senescence. The present study investigated whether an induction of autophagy and cellular senescence can be observed in oxidative-stressed keratinocytes to allow those cells to maintain a cytoprotecitve state. We examined that the effect of various inhibitors on the induction of both autophagy and senescence in H2O2-treated HaCaT cells via Western blotting and immunocytochemical assays. H2O2-treated cells exhibited increased expression of the senescent markers, p21 and Decades (Dec1), in addition to increased and decreased numbers of senescence-associated β-galactosidase (SA-β-gal) – and Ki-67–positive cells, respectively. These senescent cells also displayed upregulation of the autophagy marker, LC3-II. Attenuation of LC3-II expression using 3-methyladenin inhibited H2O2- autophagy and cellular senescence. Our Western blotting results revealed that H2O2-induced autophagy was regulated independently by the negative feedback pathway of a mammalian target of rapamycin. By contrast, H2O2-induced autophagy and cellular senescence depended on the activation of the p38 mitogen-activated protein kinase α (MAPKα) pathway mediated by the intracellular reactive oxygen species (ROS) production. Furthermore, a suppression of autophagy by 3-methyladenine promoted an induction of apoptosis in H2O2-treated cells, suggesting that autophagy, in association with the cellular senescence, may induce the cytoprotection under the oxidative stress. Our findings suggest that the acceleration of both events may allow stressed cells to maintain the cytoprotective effects and may be regulated, in part, by p38 MAPK activation through the intracellular production of ROS.</p>

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