| Project/Area Number |
16H06641
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
Fujino Naoya 東北大学, 大学病院, 助教 (10633670)
|
|---|
| Project Period (FY) |
2016-08-26 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | 気道上皮細胞 / 炎症 / Axl受容体チロシンキナーゼ / 慢性閉塞性肺疾患 / 組織幹細胞 / 気道上皮 / リモデリング / 受容体チロシンキナーゼ / 細胞・組織 / シグナル伝達 / 再生医学 / 発現制御 |
|---|
| Outline of Final Research Achievements |
Axl receptor tyrosine kinase is known to be expressed by macrophages and dendritic cells. The applicant previously found that Axl was also expressed by airway basal cells. However the role of Axl in airway basal cells of chronic obstructive pulmonary disease (COPD) has not been determined. We found that the number of Axl+/P63+ basal cells increased in COPD ex-smokers bronchioles compared to control never-smokers and control ex-smokers. In vitro experiments using human bronchial epithelial cell line Beas2B cells indicated that Axl did not regulate epithelial-to-mesenchymal transition, which was reported to be associated with cancer progression. However we found that Axl kinase regulated chemokine and cytokine expression in Beas2B cells, which promote neutrophil inflammation. These data suggested that Axl kinase in the airway has roles in cellular proliferation and regulation of inflammation.
|
