June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Novel collagen peptide inhibits choroidal neovascularization in mouse model of Wet AMD
Author Affiliations & Notes
  • Byul-Nim Ahn
    T2B infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan, Korea (the Republic of)
  • Dae-Young Hur
    T2B infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan, Korea (the Republic of)
    Anatomy and Cell Biology, Inje University College of Medicine, Busan, Korea (the Republic of)
  • Si-Kyung Kim
    T2B infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan, Korea (the Republic of)
  • Yerin Shin
    T2B infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan, Korea (the Republic of)
  • Jae Wook Yang
    T2B infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan, Korea (the Republic of)
    Department of Ophthalmology, Inje University College of Medicine, Busan, Korea (the Republic of)
  • Footnotes
    Commercial Relationships   Byul-Nim Ahn, None; Dae-Young Hur, None; Si-Kyung Kim , None; Yerin Shin, None; Jae Wook Yang, None
  • Footnotes
    Support  This study was supported by a grant from the Korea Healthcare Technology R&D Project, Ministry of Health and Welfare Affairs, Republic of Korea
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 1932. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Byul-Nim Ahn, Dae-Young Hur, Si-Kyung Kim, Yerin Shin, Jae Wook Yang; Novel collagen peptide inhibits choroidal neovascularization in mouse model of Wet AMD
      . Invest. Ophthalmol. Vis. Sci. 2017;58(8):1932.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose : Laser-induced choroidal neovascularization (CNV) mouse model is used world widely for wet-AMD. Laser induced CNV model relies on laser injury to rupture of Bruch’s membrane, resulting in subratinal blood vessel recruitment from the choroid, mimicking the main symptoms of human AMD. We aimed to investigate the anti-angiogenic effect of novel collagen peptide (HYP-G-Q-D-G-L-A-G-P-K) in experimental CNV mouse model.

Methods : CNV was induced in C57BL/6 mice by laser photocoagulation using image-guided laser system (Micron IV, Phoenix Research Laboratories). Intravitreal injections of aflibercept and peptide were administrated for 3 days starting at day of laser injury. After 2 weeks laser photocoagulation, CNV areas were measured on fundus fluorescein angiography (FFA), optical coherence tomography (OCT) and histopathological assay. Change of visual function was evaluated by electroretinogram (ERG). VEGF and macrophage infiltration were detected by immunohistochemistry.

Results : Two weeks after laser photocoagulation, the volume of CNV vessels increased exponentially. However, intravitreal injection of peptide decreased the size of the CNV lesions compared with vehicle (PBS) injections. H&E stained section showed that CNV size was dramatically decreased in peptide injected eye. ERG responses were found to decline with increasing size of CNV. However, injection of peptide restored the reduced ERG a- and b-wave. Peptide treatment also significantly inhibited macrophage infiltration and VEGF expression in the CNV area.

Conclusions : A novel collagen peptide reduced visual function loss and inhibited newly forming vessel and regressed CNV by macrophage infiltration and VEGF expression, suggesting that the peptide suppresses CNV through VEGF inhibition. Therefore, the collagen peptide maybe a possible promising material for treatment of wet-AMD.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

×
×

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.

×