May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Involvement of Hyarulonan With Choroidal Neovascularization
Author Affiliations & Notes
  • H. Mochimaru
    Keio Univ School of Medicine, Tokyo, Japan
    Department of Ophthalmology,
    Laboratory of Retinal Cell Biology,
  • E. Takahashi
    Keio Univ School of Medicine, Tokyo, Japan
    Division of Gene Regulation, Institute for Advanced Medical Research,
  • K. Tsubota
    Keio Univ School of Medicine, Tokyo, Japan
    Department of Ophthalmology,
  • H. Saya
    Keio Univ School of Medicine, Tokyo, Japan
    Division of Gene Regulation, Institute for Advanced Medical Research,
  • S. Ishida
    Keio Univ School of Medicine, Tokyo, Japan
    Department of Ophthalmology,
    Laboratory of Retinal Cell Biology,
  • Footnotes
    Commercial Relationships  H. Mochimaru, None; E. Takahashi, None; K. Tsubota, None; H. Saya, None; S. Ishida, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5883. doi:https://doi.org/
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    • Get Citation

      H. Mochimaru, E. Takahashi, K. Tsubota, H. Saya, S. Ishida; Involvement of Hyarulonan With Choroidal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5883. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To investigate a role of hyarulonan (HA), a key molecule for modulating inflammation, in the development of choroidal neovascularization (CNV).

Methods: : 4-methylumbelliferone (MU), an HA synthesis inhibitor, was suspended in 1% Arabic gum. The suspension was orally administered by gastric tube every day at the dose of 0.33, 1.0 or 3.0 g/kg body weight (BW). Laser photocoagulation was performed to induce CNV. One week after photocoagulation, mice were sacrificed and CNV volume was evaluated by volumetric measurements.

Results: : The development of CNV was significantly suppressed by the treatment with MU in a dose-dependent manner. MU-treated mice at the dose of 1.0 or 3.0 g/kg BW showed a significant (P<0.01) decrease in the CNV volume (308,468±163,530 µm3 for 1.0 g/kg BW, 256,696± 148,978 µm3 for 3.0 g/kg BW) compared with vehicle-treated mice (413,722±181,960 µm3).

Keywords: inflammation • age-related macular degeneration 
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