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Roles of angiopoietin - like protein in corneal neovascularization

Research Project

Project/Area Number 21791670
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeSingle-year Grants
Research Field Ophthalmology
Research InstitutionThe 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.

Report

(3 results)
  • 2010 Annual Research Report   Final Research Report ( PDF )
  • 2009 Annual Research Report
  • Research Products

    (6 results)

All 2010 2009 2001 Other

All Presentation (5 results) Remarks (1 results)

  • [Presentation] 角膜血管新生におけるAngptl2の昨日2010

    • Author(s)
      臼井智彦
    • Organizer
      日本眼科学会
    • Place of Presentation
      名古屋
    • Year and Date
      2010-04-15
    • Related Report
      2010 Annual Research Report
  • [Presentation] Expression of angptl2 in mice corneal neovascularization2009

    • Author(s)
      Tomohiko Usui
    • Organizer
      APAO-AAO Joint congress
    • Place of Presentation
      Bali, インドネシア
    • Year and Date
      2009-05-19
    • Related Report
      2009 Annual Research Report
  • [Presentation] 角膜血管新生、リンパ管新生におけるangptl2の役割2001

    • Author(s)
      豊野哲也、臼井智彦, ほか
    • Organizer
      第115回日本眼科学会
    • Place of Presentation
      東京
    • Year and Date
      2001-05-12
    • Related Report
      2010 Final Research Report
  • [Presentation] Roles of angiopoietin like protein 2 in corneal neovascularization2001

    • Author(s)
      Usui T, et al.
    • Organizer
      ARVO annual meeting
    • Place of Presentation
      Fort Lauderdale, USA
    • Year and Date
      2001-05-06
    • Related Report
      2010 Final Research Report
  • [Presentation] 角膜血管新生におけるAngptl2の機能2001

    • Author(s)
      臼井智彦, ほか
    • Organizer
      第114回日本眼科学会
    • Place of Presentation
      名古屋
    • Year and Date
      2001-04-05
    • Related Report
      2010 Final Research Report
  • [Remarks] ホームページ等

    • Related Report
      2010 Final Research Report

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Published: 2009-04-01   Modified: 2016-04-21  

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