| Project/Area Number |
24791149
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | Hamamatsu University School of Medicine |
|---|
Principal Investigator |
KASUYA Akira 浜松医科大学, 医学部附属病院, 助教 (60599421)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 褥瘡 / 虚血再灌流 / マウスモデル / HMGB1 / 皮膚 / 虚血再潅流障害 |
|---|
| Research Abstract |
High mobility group box-1 (HMGB1) is capable of activating macrophages in injured tissues during ischemia reperfusion (IR) injury. IR is mediated through tissue ischemia, leading to excessive inflammation and enhanced skin damage. We investigated the role of HMGB1 in the experimental IR injury model. The experimental IR injury induced HMGB1 release in the epidermal keratinocytes. Furthermore, edema was found in the dermis. To investigate the role of HMGB1 on edema, we initially quantified the vascular hyperpermeability in vivo administering fluorescence-labeled nanoparticles. Next, anti-HMGB1 neutralizing antibody was administered in mice 12 hours before IR. We found that blockade of HMGB1 suppressed vascular leakage after IR and accelerated mouse wound healing in the present model. These results indicate that HMGB1 plays a crucial role in the development of cutaneous IR injury, and may be a therapeutic target for pressure ulcer.
|
