analysis of molecular mechanism in between the adipose tissue dysfunction and adipocyte progenitor differentiation
Project/Area Number |
26461140
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Cardiovascular medicine
|
Research Institution | Chiba University (2016) The University of Tokyo (2014-2015) |
Principal Investigator |
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 脂肪幹細胞 / 脂肪組織機能異常 / 脂肪新生 / メタボリックシンドローム / 慢性炎症 / 耐糖能異常 / 脂肪細胞分化 / 肥満 / 加齢 / 組織間相互作用 / 免疫細胞 |
Outline of Final Research Achievements |
Previous reports represented that the obesity has a close relations to the atherosclerotic diseases. Howevere, there are a lot of missing link in the molecular mechanisms. Here, we report that the adipocyte progenitor cells could have the unknown role in adipose tissue dysfunction. Normally, the obesity stress induces adipose progenitor cell hyperplasia. Under the stress, the adipose progenitor cells will differentiate into new cell clusters, which will produce inflammatory cytokines and have completely different gene expression profiles. We named these cells as adipocyte progenitor derived pro-inflammatory cells (APDP cells), and this APDP cell has a unique identity to induce angiogenesis in adipose tissue. We thought this unique identity should be the adaptation to the over lipid stress. And also we could say that the failure of the adaptation to the stress is the cause of inflammatory phenotype in adipose tissue.
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Report
(4 results)
Research Products
(5 results)