Abstract
Purpose:
Aldehyde dehydrogenase 3A1 (ALDH3A1) is expressed at high levels in the mammalian cornea. We have previously shown that Aldh3a1(-/-) knockout mice in a mixed genetic background develop cataracts in the anterior and posterior subcapsular regions as well as punctate opacities in the cortex by 1 month of age. In this study, we evaluated the contribution of ALDH3A1 to modulation of transparency in the mouse cornea.
Methods:
Transparency in the corneal stroma was examined in our recently-developed Aldh3a1(-/-) congenic transgenic mice bred into a C57BL/6J genetic background by in vivo confocal microscopy.
Results:
In these ALDH3A1 knockout mice, in vivo confocal microscopy revealed light scattering from stromal keratocyte cell bodies throughout the entire corneal stroma. By contrast, corneas from wild-type mice showed light scattering only from occasional keratocyte nuclei and no light scattering from the corneal stroma. To more highly resolve the loci of corneal light scattering, live corneas were scanned using laser scanning confocal microscopy. In wild-type mice, the corneal stroma showed scattering from corneal nerves and occasional keratocyte nuclei. In the ALDH3A1 knockout mice, marked light scattering over the keratocyte cell bodies, suggesting intracellular light scattering, a phenomenon not detected in normal keratocytes.
Conclusions:
Overall, these findings indicate that the corneal keratocytes from ALDH3A1 knockout mice show elevated light scattering relative to wild-type mice. The finding that the light scattering appeared to be discrete within the keratocytes rather than diffuse, suggests that the loss of ALDH3A1 leads to increased light scattering from structures within the cell rather than from a change in the cellular refractive index. Accordingly, it would appear that ALDH3A1 may function to prevent corneal hazing by reducing intracellular keratocyte light scattering.
Keywords: 484 cornea: stroma and keratocytes •
488 crystallins •
740 transgenics/knock-outs