| Project/Area Number |
23791281
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | Oita University |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
FUJIWARA Sakuhei 大分大学, 医学部皮膚科, 教授 (90181411)
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
|---|
| Keywords | アクチン / エピプラキン / 細胞遊走 / 発現抑制 / HeLa 細胞 / 細胞内シグナル |
|---|
| Research Abstract |
To study the function of EPPK, we developed EPPK knock-down (KD) and EPPK-overexpressing HeLa cells and analyzed cellular phenotypes and motility by fluorescence/ differential interference contrast time-lapse microscopy and immunolocalization of actin and vimentin. Cellular motility of EPPK-KD cells was significantly elevated, but that of EPPK-overexpressing cells was obviously depressed. Many spike-like projections were observed on EPPK-KD cells, with fewer such structures on overexpressing cells. By contrast, in EPPK-KD cells, expression of E-cadherin was unchanged but vimentin fibers were thinner and sparser than in controls, and they were more concentrated at the peri -nucleus, as observed in migrating keratinocytes at wound edges in EPPK-/-mice. Our results suggest that EPPK is associated with the machinery for cellular motility and contributes to tissue architecture via the rearrangement of intermediate filaments.
|
