Fig. 8: Uveitic Glaucoma-like features in Yap cKO mice.
From: Uveitic glaucoma-like features in Yap conditional knockout mice
Yap deletion in both Müller glia and NPE cells of the ciliary body leads to defects in homeostatic key functions. This eventually results in the development of a glaucoma-like phenotype. Within the anterior chamber, Yap cKO mice harbor breakdown of the blood-aqueous barrier starting by 2 months (2 M) of age at the iris level, and distension of ciliary processes. The ciliary body then further degenerates until complete collapse at 9 months (9 M) of age. At the retinal level, early defects include downregulation of Müller cell proteins like GS, vascular defects, and optic nerve head deformation. This is followed along with aging by reactive gliosis, deregulation of glutamate homeostasis and RGC death. AC anterior chamber, CB ciliary body, CP ciliary processes, GCL ganglion cell layer, INL inner nuclear layer, ONH optic nerve head, ONL outer nuclear layer, PC posterior chamber, RGC retinal ganglion cells, RNFL retinal nerve fiber layer.
