May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Experimental Retinal Neovascularization in MMP-2 Knock Out Mice
Author Affiliations & Notes
  • S. Sarman Sejersen
    St. Erik's Eye Hospital, Department of Clinical Sciences, Karolinska Institute, Stockholm, Sweden
  • I. van der Ploeg
    St. Erik's Eye Hospital, Department of Clinical Sciences, Karolinska Institute, Stockholm, Sweden
  • A. Kvanta
    Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden
  • Footnotes
    Commercial Relationships  S. Sarman Sejersen, None; I. van der Ploeg, None; A. Kvanta, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2908. doi:
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      S. Sarman Sejersen, I. van der Ploeg, A. Kvanta; Experimental Retinal Neovascularization in MMP-2 Knock Out Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2908.

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

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Abstract: : Purpose: Previous studies have shown that matrix metalloproteinase-2 (MMP-2) is involved in experimental, inflammation-associated, choroidal neovascularization (Berglin et al. IOVS, in press). To investigate whether MMP-2 is also involved in experimental, ischemia-associated, retinal neovascularization we have studied neovascularization in a model for retinopathy of prematurity (ROP) in MMP-2 knock out mice. Methods: Ischemic retinopathy was produced in 14 MMP-2 knock out mice and 20 control mice. 7-day-old pups were exposed to 75% 02 for 5 days and then returned to normoxic conditions for an additional 5 days. Retinal neovascularization was maximal at P17 when mice were sacrified and eyes were enucleated and fixed. Serial paraffin embedded sections were stained with hematoxylin-eosin and neovascularization was quantified by counting the number of retinal vascular cell nuclei internal to the inner limiting membrane. Retinal neovascularization was also visualized on retinal flat-mounts from animals perfused with FITC-dextran. Results: In the MMP-2 knock out mice group the median number of nuclei on the vitreous side of ILM was 26,0 (range 16,4 - 49,1) compared to 35,8 (range13,6 - 67,4) in the control mice group. Retinal neovascularization was non-significantly reduced in the MMP-2 knock out mice group. Retinal flatmounts appeared similar in the two groups. Conclusions: The weak and statistically non-significant reduction in retinal neovascularization in MMP-2 knock out mice compared to normal mice suggests that MMP-2 may be less important in ischemia-associated neovascularization.

Keywords: retinal neovascularization • neovascularization • molecular biology 

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