2016 Fiscal Year Final Research Report
Role of PLC epsilon-PKC myu pathway in skin inflammation, skin cancer, cataract, and psoriasis vulgaris.
Project/Area Number |
26461692
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Tohoku Medical and Pharmaceutical University (2016) Kobe University (2014-2015) |
Principal Investigator |
OKA Masahiro 東北医科薬科大学, 医学部, 教授 (30252761)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | 尋常性乾癬 / ホスホリパーゼCε / プロテインキナーゼCμ / マウス / 皮膚 / 紫外線発がん / 創傷治癒 |
Outline of Final Research Achievements |
Phospholipase C (PLC) epsilon is a phosphoinositide-specific PLC regulated by small GTPases including Ras and Rap. In order to investigate the role of PLC epsilon in the skin, we created transgenic mice over expressing PLC epsilon in epidermal leratinocytes. The resulting transgenic mice spontaneously developed skin inflammation like psoriasis vulgaris as characterized by formation of adherent silvery scales, acanthosis, parakeratosis, and infiltration of neutrophils in the epidermis, and aberrant infiltration of immune cells such as T cells and dendritic cells. After observing that protein kinase C μ (PKCμ) is activated after activation of PLC epsilon, we created transgenic mice overexpressing PKCμ in epidermal leratinocytes (K5-PKCμ-TG). However, the K5-PKCμ-TG did not show skin changes seen in psoriasis vulgaris. These results indicate that overexpression of PLC epsilon induces psoriasis-like skin changes but these changes are not mediated by PKCμ.
|
Free Research Field |
皮膚科学
|