| Project/Area Number |
21791060
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
ISHII Yoshiyuki University of Tsukuba, 大学院・人間総合科学研究科, 講師 (90455931)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 紫外線障害 / A170 / Sequestosomel / p62 / アポトーシス |
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| Research Abstract |
In this study, the role of A170 in UVB induced apoptosis was investigated. A170 is known to stress inducible gene, and A170 deficient mice show mature onset obesity. We previously found mouse embryonic fibroblast (MEF) derived from A170 KO mice were resistant to UVB induced cell death. At first, we analyzed whether A170 knocked down wild type MEF show same characters as KO MEF against UVB radiation. The results shows knockdown cells are also resistant to UVB. Next, the proteins involved in the apoptotic signal were analyzed. Interestingly, pro-apoptotic protein levels such as Bax, caspase after UVB exposure were reduced in KO cells. In addition, anti-apoptotic protein mRNA levels were markedly increased in KO cells compared with WT. We found transcription factor Stat3 which is known to positively regulates anti-apoptotic gene induction was remarkably activated in KO cells. Moreover, in vivo analysis revealed that A170 KO mice skin tissue show relatively low damage by UVB radiation. These results suggest that A170 is novel important factor for regulating apoptotic signal by altering pro- and anti-apoptotic protein levels.
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