| Project/Area Number |
25460505
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Experimental pathology
|
|---|
| Research Institution | Kanazawa Medical University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YOSHIZAKI Hisayoshi 金沢医科大学, 医学部, 講師 (00443490)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 細胞間接着 / 低分子量G蛋白質 / 細胞形態 / 極性 / 増殖因子 / 上皮細胞 |
|---|
| Outline of Final Research Achievements |
Rupture of lens cataract (RLC) mouse showed spontaneous rupture of the lens capsule at the posterior pole, followed by dislocation of the inner nucleus. We showed previously that the Dock5 protein was hardly detectable in the RLC mice, while the Dock5 mRNA was expressed. Firstly, we observed H&E stained eyes from the wild-type BALB/c and RLC mice. We found the gap between the lens epithelial cells (LECs) and fiber cells at 3-week-old RLC and DOCK5 knock-out mice. Pathway analysis revealed that genes related to inflammatory response and lipid metabolism are altered in RLC mice.
To reconstitute the LEC in vitro, we tried to isolate the LEC from the mice to culture them. However, addition of sera induced epithelial mesenchymal transition of LEC. We also found the human and mouse cell lines lost E-Cadherin expression or apico-basal polarity. Interestingly in those cell lines, DOCK180 is expressed.
|
