Purchase this article with an account.
C. T. Fu, T. Tran, D. Sretavan; Upregulation of EphB2 Expression in an Experimental Model of Ocular Hypertension in CD1 Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3680.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To evaluate an experimental model of ocular hypertension induced by laser photocoagulation in albino CD1 mice, and to examine the change of EphB2 expression at the optic nerve head (ONH) following intraocular pressure (IOP) elevation.
Experimental ocular hypertension was induced unilaterally in adult albino CD1 mice by laser photocoagulation of limbal and episcleral veins (532nm wavelength, 150mW power, 0.5 second duration, 100 um diameter spot size). IOP in both eyes was measured with a Tonolab tonometer at 1 day, 2 days, 1 week 2 weeks, and 4 weeks following laser treatment. At 4 weeks, retinal whole-mounts were immunostained using the retinal ganglion cell (RGC) marker Brn-3b. Labeled RGCs were imaged with the Zeiss LSM 5 Pascal microscope and counted using an image analysis software (ImageJ). Expression of the EphB2 receptor tyrosine kinase was examined by mRNA in situ hybridization in ONH tissue sections harvested at 1 week after treatment.
IOP significantly increased in laser-treated eyes at 1 day (29.24 mmHg) and 2 days (28.92 mmHg) following surgery compared to contralateral control eyes (13.08 mmHg), and declined to baseline level (15.40 mmHg) by 1 week. Despite normalization of IOP, Brn-3b positive RGC density in experimental eyes was reduced to approximately 11% of controls at 4 weeks. Upregulation of EphB2 mRNA was detected at the ONH of operative eyes as early as 1 week, which preceded substantial RGC loss.
Laser photocoagulation of limbal and episcleral veins in CD1 mice causes IOP elevation and RGC loss. The upregulation of EphB2 expression at the ONH documented in this study is consistent with that previously reported in DBA/2J mice, a genetic mouse model of pigmentary glaucoma. Furthermore, EphB2 upregulation preceded widespread RGC loss, suggesting a potential functional role of this molecule in modifying the development and/or progression of glaucomatous disease.
This PDF is available to Subscribers Only