April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
The Role of Heparan Sulfate in Oxgen-Induced Retinopathy
Author Affiliations & Notes
  • K. M. Nishiguchi
    Ophthalmology, Nagoya Univ Sch Med, Nagoya, Japan
  • K. Kataoka
    Ophthalmology, Nagoya Univ Sch Med, Nagoya, Japan
  • S. Kachi
    Ophthalmology, Nagoya Univ Sch Med, Nagoya, Japan
  • H. Terasaki
    Ophthalmology, Nagoya Univ Sch Med, Nagoya, Japan
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3349. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      K. M. Nishiguchi, K. Kataoka, S. Kachi, H. Terasaki; The Role of Heparan Sulfate in Oxgen-Induced Retinopathy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3349.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : To examine the role of heparan sulfate (HS) in the ocular fluid during physiological and pathological retinal neovascularization.

Methods: : The concentration of HS in aqueous humor from C57BL mice at post-natal day 7 (P7), P12, P17, and P60 were determined with Enzyme-Linked Immuno-Sorbent Assay. The HS levels of serum and urine were also analyzed at P17. After C57BL mice were exposed to 80% oxygen from P7 to P12, they were housed in room air for 5 days, which resulted in the development of oxygen-induced retinopathy (OIR). The HS concentrations of aqueous humor were measured at P12 and P17 during the course of OIR development. Phosphate buffered saline (PBS) or Heparinase III, an enzyme that specifically degrades HS, was injected into the eyes at P3 in wild-type mice or at P12 after 5 days’ exposure to 80% oxygen in OIR model. The retinal specimens collected at P8 and P17 were stained with Griffon simplicifolia. Their vascular structures were evaluated with retinal flatmounts.

Results: : The HS concentrations of wild-type aqueous humor were 732 ± 74, 1470 ± 110, 1824 ± 77, and 115 ± 25 µg/ml (mean ± S.E.M.) at P7, P12, P17, and P60, respectively. The HS level was higher in aqueous humor than that of serum (10.2 ± 2.9 µg/ml) or urine (7.7 ± 1.3 µg/ml) collected from the same mice at P17. The HS concentrations were not different between aqueous humor from wild-type and OIR mice at P12 (1283 ± 91 µg/ml) or P17 (1648 ± 74 µg/ml). In OIR mice, the area of neovascularization was significantly increased (P = 0.002) in the eyes injected with Heparinase III (8.5 ± 0.9%: mean ± S.E.M.) compared to those injected with PBS (3.9 ± 0.5%). The vascularized area of wild-type retina was not different at P8 between eyes injected with Heparinase III (88.0 ± 0.9%) and PBS (85.8 ± 2.0%) at P3.

Conclusions: : HS may serve as an endogenous inhibitor of non-physiological neovascularization in neonatal retinovascular diseases.

Keywords: retinal neovascularization • vascular endothelial growth factor • glycoconjugates/glycoproteins 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×