December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Squalamine Lactate Inhibits Choroidal Neovascular Membrane (CNVM) Formation in a Rat Laser-Trauma Model
Author Affiliations & Notes
  • MH Criswell
    Retina Service Research Laboratories Department of Ophthalmology Indiana University School of Medicine Indianapolis IN
  • TA Ciulla
    Retina Service Research Laboratories Department of Ophthalmology Indiana University School of Medicine Indianapolis IN
  • RP Danis
    Retina Service Research Laboratories Department of Ophthalmology Indiana University School of Medicine Indianapolis IN
  • JI Williams
    Genaera Corporation Plymouth Meeting PA
  • MP McLane
    Genaera Corporation Plymouth Meeting PA
  • KJ Holroyd
    Genaera Corporation Plymouth Meeting PA
  • Footnotes
    Commercial Relationships    M.H. Criswell, Genaera Corporation F; T.A. Ciulla, Genaera Corporation F; R.P. Danis, Genaera Corporation F; J.I. Williams, Genaera Corporation E; M.P. McLane, Genaera Corporation E; K.J. Holroyd, Genaera Corporation E. Grant Identification: Genaera Corporation and an unrestricted grant from Research to Prevent Blindness, Inc.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1264. doi:
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    • Get Citation

      MH Criswell, TA Ciulla, RP Danis, JI Williams, MP McLane, KJ Holroyd; Squalamine Lactate Inhibits Choroidal Neovascular Membrane (CNVM) Formation in a Rat Laser-Trauma Model . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1264.

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

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Abstract

Abstract: : Purpose: Squalamine is an aminosterol, originally isolated from the tissues of the dogfish shark, which exhibits low systemic toxicity and which recently demonstrated antiangiogenic effects in a mouse model of retinopathy of prematurity (Higgins, R.D., et al., Invest Ophthalmol Vis Sci. 2000; 41:1507). Here we characterize the inhibitory effects of squalamine on CNVM formation in a rat laser-trauma CNVM model. Methods: A series of 8 concentrically-arranged lesion sites was placed bilaterally around the optic disks of 20 Brown Norway rats using a krypton red laser (Coherent: 647 nm, 0.05 sec, 150 mW, 50 µm). Following lesion induction, 10 rats immediately began to receive a series of systemic intraperitoneal injections of squalamine (dosage: 5mg/kg/injection, b.i.d.) for 9 days out of the 28 day experimental period. The remaining 10 control rats received similar injections that contained only D5W. Follow up fundus, fluorescein angiography (FA), and tissue histology examinations were conducted. Results: Fundus and FA yielded only subtle indications of differences between the two groups. Histologic analysis of lesion sites revealed partial, but significant (p < 0.001) inhibition of CNVM mean thickness of the squalamine-treated group (47 ± 11 mm), as compared to the mean thickness (63 ± 14 mm) of the control group. Conceivably, the initial time for systemic squalamine levels to develop versus the fast and aggressive CNVM development characteristics of this particular animal model may have partially masked the overall efficacy of squalamine. Conclusion: Systemically administered squalamine lactate partially inhibits neovascular development in this CNVM rat model. In conjunction with other existing and developing therapies, squalamine may have a potential role in the treatment of human CNVM formation.

Keywords: 346 choroid: neovascularization • 390 drug toxicity/drug effects • 316 animal model 
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