Project/Area Number |
09670869
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Kanazawa University |
Principal Investigator |
KAWARA Shigeru University Hospital, Faculty of Medicine, Kanazawa University, Lecturer, 医学部・附属病院, 講師 (80186155)
|
Co-Investigator(Kenkyū-buntansha) |
TAKAHARA Kazuhiko Faculty of Medicine, Kanazawa University, Professor, 医学部, 教授 (50142253)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
Keywords | Ultraviolet rays / Transforming growth factor-beta / Cyclin / Cell proliferation / Epidermis / 形質転換成長因子-β / 形質転換増殖因子β |
Research Abstract |
In these studies, we investigated the effects of TGF- beta on epidermal injury due to chronic ultraviolet exposures in hairless mice. In mice with a single exposure of ultraviolet BETA(UVB)(200mJ/cm^2), TGF- beta and receptors to TGF - beta were strongly expressed in the epidermis during 1-6 hours after an exposure, with the decrease of labeling indices. During the same period, the transfer of Smad2/3 to nuclei and the increase of p21 positive cells were observed in the epidermis. At 12-24 hours after an exposure, labeling indices showed an increase with the increase of cyclin E-positive cells. From those results, it was suggested that TGF- beta played an important role on the cell cycle regulation accompanied with DNA injury due to UVB. Repeated exposures of UVB induced the continuous increase of labeling indices. In mice with repeated exposures of UVB, the expressions of TGF- beta, receptors to TGF- beta and p21 were observed at 6weeks after the discontinuation of exposures. Those results suggested that the abnormal regulation of TGF- beta on the cell cycle due to repeated exposures of UVB was responsible for chronic injury of the epidermis, including the UV-induced cancer.
|