| Project/Area Number |
16K19462
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | Yokohama City University |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
Hogan Brigid L. M.
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 組織幹細胞 / 気道上皮修復 / 上皮ー間質相互作用 / 基底幹細胞 / BMPシグナル / 細胞増殖制御 / 細胞脱落 / 気道上皮 / 幹細胞ニッチ / Bmpシグナル / 細胞・組織 / 再生医学 / 発生・分化 / シグナル伝達 |
|---|
| Outline of Final Research Achievements |
The airway epithelium is mainly composed of ciliated and secretory luminal cells. Basal stem cells self-renew and give rise to luminal cells at steady state and after injury. Using the 3D organoid culture system and in vivo gas injury model, it is revealed that BMP from the mesenchyme places a break on the proliferation of the epithelium at steady state. This break is released transiently during repair by the upregulation of BMP antagonists. As repair proceeds, cell density increases almost twofold over steady state because of an accumulation of suprabasal cells. If the BMP antagonist is given during repair, the maximum cell number is increased over controls. However, during the next phase of repair the density of epithelial cells is restored by the active extrusion of apoptotic cells. Taken together, these results reveal a critical role for both BMP signaling and cell shedding in homeostasis of the airway epithelium.
|
