2015 Fiscal Year Final Research Report
The mechanism to maintain the lens epithelial cell morphology.
| 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
|
| Keywords | 細胞間接着 / 低分子量G蛋白質 |
|---|
| 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.
|
| Free Research Field |
実験病理
|
