Myeloid cell dysfunction and the pathogenesis of ovarian hypertrophy.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04693
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: Akita University
• Principal Investigator: Sasaki Junko 秋田大学, 医学(系)研究科(研究院), 准教授 (30333371)
• Co-Investigator(Renkei-kenkyūsha): NAKANISHI HIROKI 秋田大学, 大学生体情報研究センター, 助教 (10466740)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 細胞内シグナル伝達 / イノシトールリン脂質

Outline of Final Research Achievements

In this study we analyzed the relationship between aberrant lipid metabolism and the pathogenesis of ovarian hypertrophy using myeloid cell-specific phosphoinositide metabolizing enzymes-deficient mice (cDKO mice). We found that ovarian hypertrophy in cDKO mouse was induced by a high PIP3 level and Akt hyperactivation, and not only conventional myeloid cells but also uncharacterized cells contributed to the disease pathogenesis.

Free Research Field

脂質生化学