March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Retinal Ganglion Cell Loss Correlates With Increased IOP in MMP-9 Knockout Mice
Author Affiliations & Notes
  • Behrad Garmsiri
    Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
  • Jennifer V. Robertson
    Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
  • Alexander K. Ball
    Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
  • Judy A. West-Mays
    Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada
  • Footnotes
    Commercial Relationships  Behrad Garmsiri, None; Jennifer V. Robertson, None; Alexander K. Ball, None; Judy A. West-Mays, None
  • Footnotes
    Support  American Health Assistance Foundation (JWM)
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6942. doi:
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    • Get Citation

      Behrad Garmsiri, Jennifer V. Robertson, Alexander K. Ball, Judy A. West-Mays; Retinal Ganglion Cell Loss Correlates With Increased IOP in MMP-9 Knockout Mice. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6942.

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

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Abstract

Purpose: : Matrix metalloproteinases (MMPs) are endopeptidases that degrade the retinal ganglion cell (RGC) layer extracellular matrix after injury to RGCs. Retinal MMP-9 is upregulated in ischemia, NMDA excitotoxicity, and elevated intraocular pressure (IOP) associated RGC death. Abnormal expression of MMP-9 has recently been implicated in the etiology of glaucoma. We have previously reported that IOP is elevated in MMP-9 knock out (KO) mice. The purpose of this study was to examine RGC survival in MMP-9 KO mice after several weeks of elevated IOP.

Methods: : IOP measurements were made in anaesthetized (Avertin) 3-4 month old MMP-9 KO mice on a C57BL/6 background and age-matched wild type (WT) littermates using rebound tonometry (TonoLab). Full-field Electroretinograms (ERGs) were recorded to evaluate the amplitude of the a-wave, b-wave (distal retina), and scotopic threshold response (STR; proximal retina) in both KO and WT mice. The mice were euthanized and their eyes fixed in phosphate buffered 4% formaldehyde, washed, and retinas removed. Retinas were incubated in goat∝Brn3 (c-13; Santa Cruz; 1:500) to label RGCs and rabbit∝PGP9.5 (UltraClone; 1:500) to label amacrine cells and RGCs in the RGC layer. RGCs and all neurons in the midperiphery of each quadrant of the RGC layer were counted in flatmounted retinas.

Results: : It has been reported that Brn3 antisera labels 85% of retrograded labeled RGCs from the superior colliculus in mice and is not downregulated in surviving RGCs after injury. We counted 2066±413 Brn3 immunoreactive (-IR) cells/mm² in WT retinas, and only 1283±257 Brn3 cells/mm² in the MMP-9 KO mice, which had a sustained 20% increase in IOP sustained over several weeks. There was a significant (t-test) 38% decrease in RGCs, which is equivalent to the loss seen in mice 7 days after optic nerve transection. The retina was otherwise normal. There was an insignificant (ANOVA), but expected decrease in PGP9.5-IR neurons in the RGC layer (WT: 4612±333 vs KO: 4291±393 cells/mm²) indicating that the only cells affected were Brn3-IR RGCs. There was also no significant change in a- or b-wave ERG amplitudes, suggesting that the distal retinal neurons were functionally normal. There was no significant difference in the STR due to high variability in this response. A Pearson correlation analysis showed that there was a strong correlation between the number of surviving Brn3-IR RGCs and the increase in IOP (0.749; P=0.05).

Conclusions: : Our results demonstrate that MMP-9 KO mice have elevated IOPs that correlate with a specific loss of RGCs. An impaired ability to remodel the ECM by eliminating MMP-9 activity did not ameliorate RGC loss in these animals. These findings implicate MMP-9 in the development of high IOP and RGC loss in a mouse model of glaucoma.

Keywords: ganglion cells • intraocular pressure • electroretinography: non-clinical 
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