Pathogenetic machanism for pyoderma gangrenosusm by disruption of the production pathway of phosphatidylinositol (3,5) biphosphate

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670518
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Dermatology
• Research Institution: Akita University
• Principal Investigator: Hasunuma Naoko 秋田大学, 医学部, その他 (10282170)
• Co-Investigator(Renkei-kenkyūsha): Manabe Motomu 秋田大学, 大学院医学系研究科, 教授 (30138309) ; Horie Yasuo 秋田大学, 大学院医学系研究科, 講師 (30282164)
• Research Collaborator: SUZUKI Tomoko ; KAGAYA Masami
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 壊疽性膿皮症 / イノシトールリン脂質 / ノックアウトマウス / 炎症性皮膚疾患 / 細胞内小胞輸送系

Outline of Final Research Achievements

Pyoderma gangrenosum is a chronic inflammatory skin disease of unknown etiology. To investigate the pathogenic mechanism for pyoderma gangrenosum, we generated mutant mice harboring epidermal specific deletion of type III phosphatidylinositol phosphate kinase (PipkIII). However, the mutant mice died several hours after birth. To overcome this neonatal death and to examine functional roles of PipkIII in the epidermis, we then generated tamoxifen-inducible PipkIII-deficient mice. After tamoxifen application, we found that intensive vacuolization occurred in the epidemis and follicular epithelium. However, we failed to detect dense neutrophilic infiltration in the dermis, which is a characteristic histopathological feature of pyoderma gangrenosum, in the mutant mice. We will examine the role of PipkIII in intracellular transport in the epidermis.

Free Research Field

皮膚科学