2015 Fiscal Year Final Research Report
Darier disease- possible therapeutic approach for ultraviolet B-induced aggravation.
| Project/Area Number |
26860896
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAGI Atsushi 順天堂大学, 医学部, 非常勤講師 (40459160)
IKEDA Shigaku 順天堂大学, 医学部, 教授 (40193198)
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| Research Collaborator |
WADA Akino
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | 皮膚科学 / 紫外線 / ダリエー病 / プロスタグランジン |
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| Outline of Final Research Achievements |
Darier disease (DD) is an autosomal dominant inherited skin disorder. A responsible gene for DD is the human ATP2A2 gene encoding SERCA2 which transports Ca2+ from the cytoplasm into reservoirs in the ER. Ultraviolet (UV) B exposure is supposed to be one of the major aggravating factors of DD. Neither treatment of normal human keratinocytes(NHKs) with EP4 antagonist before and after UV irradiation nor simple administration of EP4 agonist influenced on ATP2A2 mRNA level. Instead, EP4 siRNA reduced EP4, UVB irradiation markedly increased EP4 , and the UVB-induced increment of EP4 was also suppressed by EP4 siRNA in a protein level. Although UVB irradiation downreguled ATP2A2 in mRNA level, the UVB-mediated downregulation of ATP2A2 mRNA was recovered by EP4 siRNA introduction.The result was also confirmed in SERCA2 protein level. These findings indicated that EP4 receptor is involved in UVB-mediated downregulation of ATP2A2/SERCA2 via PGE2-EP4 signaling in NHKs.
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| Free Research Field |
角化異常症
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