| 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 |
|
|---|
| 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
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | オートファジー / アポトーシス / 紫外線 / ストレス / 皮膚 / マイトファジー / 表皮ケラチノサイト / 紫外線照射 / 酸化ストレス / MAPキナーゼ / 皮膚表皮 / 形態形成 / UV |
|---|
| 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.
|
