June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
Corneal abnormalities in the DBA/2J mouse model of glaucoma: DBA/2J-Gpnmb+/SjJ as a critical control
Author Affiliations & Notes
  • Landon James Rohowetz
    Ophthalmology, University of Missouri Kansas City Vision Research Center, Kansas City, Missouri, United States
  • Sean Riordan
    Ophthalmology, University of Missouri Kansas City Vision Research Center, Kansas City, Missouri, United States
  • Peter Koulen
    Ophthalmology, University of Missouri Kansas City Vision Research Center, Kansas City, Missouri, United States
    Biomedical Sciences, University of Missouri Kansas City School of Medicine, Kansas City, Missouri, United States
  • Footnotes
    Commercial Relationships   Landon Rohowetz, None; Sean Riordan, None; Peter Koulen, None
  • Footnotes
    Support  NIH: EY022774, RR27093, EY031248 (PK); Felix and Carmen Sabates Missouri Endowed Chair in Vision Research (PK); Challenge Grant from Research to Prevent Blindness (PK); In memory of Dr. Larry Piebenga by the Dawe Family Foundation (PK).
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 2353. doi:
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    • Get Citation

      Landon James Rohowetz, Sean Riordan, Peter Koulen; Corneal abnormalities in the DBA/2J mouse model of glaucoma: DBA/2J-Gpnmb+/SjJ as a critical control. Invest. Ophthalmol. Vis. Sci. 2021;62(8):2353.

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

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Abstract

Purpose : The DBA/2J (D2) mouse strain is widely used as a model for glaucoma. We compared the D2 and DBA/2J-Gpnmb+/SjJ (D2G) mouse strains to determine the relative roles of age-related changes in IOP and corneal pathology on visual dysfunction in the D2 mouse model of glaucoma. D2G mice are genetically identical to D2 mice with the exception of a normally functioning Gpnmb gene resulting in a lack of iris pigment dispersion and the absence of IOP elevation and glaucomatous neuropathy.

Methods : IOP, visual acuity (VA) and corneal calcification were studied in D2 and D2G mice. IOP and VA were monitored over a 12-month period using tonometry and behavioral measures of the optomotor reflex. At 6, 9 and 12 months, corneas from each group were examined using confocal microscopy to measure the intensity, thickness and size of calcified regions.

Results : D2 mice developed elevated IOP between 9 (13.53 ± 0.88 mmHg) and 12 months of age (23.53 ± 1.72 mmHg), but D2G mice did not (12.34 ± 0.33 mmHg at 9 and 13.8 ± 0.47 mmHg at 12 months). Corneal calcification was found in 46.4% of D2 eyes and 56.7% of D2G eyes at 6 months (P = 0.323), 52.5% and 52.6% at 9 months (P = 0.991) and 83.3% and 60.0% at 12 months (P = 0.1113). When comparing 9 and 12 month-old mice with calcification, D2 mice demonstrated an increase in calcification thickness (P = 0.005) and D2G mice demonstrated increases in calcification intensity (P = 0.006) and thickness (P = 0.036). At 12 months of age, D2 mice with corneal calcification had greater mean IOP (25.38 ± 1.85 mmHg) than D2 mice without corneal calcification (17.5 ± 2.53 mmHg; P = 0.048). No difference in IOP was observed between D2G mice with and without calcification at any age. Calcification thickness correlated positively with IOP (r = 0.415, P = 0.004) and negatively with visual acuity (r = -0.451, P = 0.014) in D2 but not D2G mice.

Conclusions : Corneal calcification may affect noninvasive IOP measurements and visual function in D2 mice. While ocular hypertension secondary to iris pigment dispersion causes visual dysfunction, corneal abnormalities, such as corneal calcification, should be considered as potentially confounding factors for the assessment of vision loss in D2 mice.

This is a 2021 ARVO Annual Meeting abstract.

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