2017 Fiscal Year Final Research Report
Maintenance mechanism of epidermal homeostasis and its failure- Functional analysis of MCL1 in keratinocyte differentiation-
| Project/Area Number |
26461669
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
MAKINO EIICHI 川崎医科大学, 医学部, 講師 (90314674)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | MCL1 / 表皮角化細胞 / 分化 / ホメオスタシス / アポトーシス |
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| Outline of Final Research Achievements |
We successfully generated two kinds of MCL1 conditional knockout (cKO) mice, K5-Cre: MCL1flox / flox mouse and K14-CreERT2: MCL1flox / flox mouse.In these mice, Cre recombinase was induced using the tissue specific promoters of keratin 5 (K5) and keratin 14 (K14) ,which were strongly expressed in epidermal basal cells, and as a result, the flox allele of MCL1 is missing.
In the MCL1 cKO mouse, marked hyperkeratosis and epidermal hyperplasia were observed in the skin as compared with the control mouse, but clear findings of apoptosis were not obtained.Immunostaining of MCL1 revealed that MCL1 expression was maximal in the stratum corneum in normal skin tissues and MCL1 expression was not observed in the basal layer.
Interestingly, these results suggest that MCL1 may exert some function in the terminal differentiation process of epidermal cells.
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| Free Research Field |
皮膚科学
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