Roles of angiopoietin - like protein in corneal neovascularization
Project/Area Number |
21791670
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Ophthalmology
|
Research Institution | The University of Tokyo |
Principal Investigator |
USUI Tomohiko The University of Tokyo, 医学部附属病院, 助教 (80282557)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | 角膜 / 血管新生 / 炎症 / リンパ管新生 |
Research Abstract |
Cornea is transparent, avascular, and alymphatic tissue, which form outer shell of eyeball. Neovascularization of the cornea disturbs its transparency and vision secondary to a variety of corneal insults, including inflammatory corneal diseases. However, the mechanisms of corneal hemangiogensis and lymphangiogenesis have not been fully understood yet. Recently, several reports revealed that angiopoietin-like protein 2 (Angptl2) play important roles in angiogenesis of chronic inflammatory diseases and tumor. Therefore, this study focused on the roles of Angptl2 in corneal hemangiogenesis and lymphangiogenesis. The expressions of Angptl2 in normal and vascularized cornea were evaluated by RT-PCT and immunohistochemisty. Angptl2 gene expression was weakly detected in the normal mice cornea, however, the gene expression was significantly increased in vascularized corneas. In situ expression of Angptl2 was apparent in vascularized corneas. To investigate the roles of Angptl2 in inflammatory corneal neovasuclarization, we analyzed K14-Angptl2 transgenic mice and angptl2 knockout mice. Compared with wild type mice, K14-Angptl2 transgenic mice increased inflammation (macrophage infiltration), hemangiogenesis and lymphangiogenesis, otherwise, Angptl2 knockout mice decreased inflammation (macrophage infiltration), hemangiogenesis and lymphangiogenesis in mice corneal neovascularization models. Taken together, angptl2 is proinflammatoy and pro angiogenic factor in corneal neovascularization. We concluded that Angptl2 blockade could be a potent strategy to inhibit inflammatory corneal hemangiogenesis and lymphangiogenesis in corneal inflammatory diseases.
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Report
(3 results)
Research Products
(6 results)