Is autophagy involved in the protection of skin epidermis from UV induced apoptosis?

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461672
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Kindai University
• Principal Investigator: MORIYAMA Mariko 近畿大学, 薬学総合研究所, 准教授 (40595295)
• Co-Investigator(Renkei-kenkyūsha): MORIYAMA Hiroyuki 近畿大学, 薬学総合研究所, 准教授 (90581124)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: オートファジー / アポトーシス / 紫外線 / ストレス / 皮膚

Outline of Final Research Achievements

Previously, we found that BNIP3 plays a crucial role in keratinocytes differentiation by inducing autophagy. Furthermore, BNIP3 has a protective effect against UVB-induced apoptosis in keratinocytes.
In this study, we found that the accumulation of reactive oxygen species (ROS) and following activation of ERK/JNK MAP kinase by UVB irradiation was sufficient to trigger the upregulation of BNIP3 expression. Moreover, BNIP3 was required for the degradation of dysfunctional mitochondria upon UVB irradiation. These data clearly indicated that BNIP3-induced autophagy, which occurs via UVB-generated ROS-mediated JNK and ERK MAPK activation, has a crucial role in the protection of the skin epidermis against UVB irradiation.

Free Research Field

皮膚科学　幹細胞生物学