Casein kinase-2 inhibition promotes retinal ganglion cell survival after acute intraocular pressure elevation

Intraocular pressure elevation can induce retinal ganglion cell death and is a clinically reversible risk factor for glaucoma,the leading cause of irreversible blindness.We previously demonstrated that casein kinase-2 inhibition can promote retinal ganglion cell survival and axonal regeneration in rats after optic nerve injury.To investigate the underlying mechanism,in the current study we increased the intraocular pressure of adult rats to 75 mmHg for 2 hours and then administered a casein kinase-2 inhibitor(4,5,6,7-tetrabromo-2-azabenzimidazole or 2-dimethylamino-4,5,6,7-tetrabromo-1H-benzimidazole)by intravitreal injection.We found that intravitreal injection of 4,5,6,7-tetrabromo-2-azabenzimidazole or 2-dimethylamino-4,5,6,7-tetrabromo-1H-benzimidazole promoted retinal ganglion cell survival and reduced the number of infiltrating macrophages.Transcriptomic analysis showed that the mitogen activated protein kinase signaling pathway was involved in the response to intraocular pressure elevation but was not modulated by the casein kinase-2 inhibitors.Furthermore,casein kinase-2 inhibition downregulated the expression of genes(Cck,Htrsa,Nef1,Htrlb,Prph,Chat,Slc18a3,Slc5a7,Scn1b,Crybb2,Tsga10ip,and Vstm21)involved in intraocular pressure elevation.Our data indicate that inhibition of casein kinase-2 can enhance retinal ganglion cell survival in rats after acute intraocular pressure elevation via macrophage inactivation.

Bilateral retinal nerve fiber layer thickness reduction in a 9-year-old myopic boy suffering from unilateral optic neuritis:A case report

BACKGROUND In this paper,we present a 9-year-old boy who demonstrates a complex interplay between myopia progression,axial length(AL)extension,and retinal nerve fiber layer(RNFL)thickness loss in both eyes.Additionally,concurrent optic neuritis has directly impacted RNFL thickness in his right eye,and its potential indirect influence on RNFL and macular ganglion cell layer(mGCL)thickness in his left eye is also noteworthy.CASE SUMMARY A 9-year-old boy with bilateral myopia presented with diminished vision and pain in his right eye due to optic neuritis,while his left eye showed pseudopapilledema.Steroid therapy improved his vision in the right eye,and 16-mo follow-up revealed recovery without recurrence despite myopia progression.Follow-up optical coherence tomography conducted 16 mo later revealed a notable thinning of the RNFL in both eyes,especially along with a reduction in mGCL thickness in the left eye.This intricate interaction between optic neuritis,myopia,and retinal changes underscores the need for comprehensive management,highlighting potential long-term visual implications in young patients.CONCLUSION The progression of myopia and AL extension led to the loss of RNFL thickness in both eyes in a 9-year-old boy.Concurrently,optic neuritis directly affected RNFL thickness in his right eye and may indirectly play a role in the thickness of RNFL and mGCL in his left eye.