Clinical outcomes of patterned laser trabeculoplasty as adjuvant therapy in open angle glaucoma and ocular hypertension

AIM： To assess the efficacy and safety of patterned laser trabeculoplasty（PLT） as an adjunctive treatment in open angle glaucoma（OAG） or ocular hypertension（OHT） patients who were under antiglaucoma medical treatment.METHODS： This study was a retrospective review of primary or secondary OAG patients and OHT patients with medically uncontrolled（≥18 mm Hg） intraocular pressure（IOP） who underwent 360o PLT from June 2016 to August 2016. Follow-up visits at week 1, and 1, 3 and 6 mo were performed. IOP, best corrected visual acuity（BCVA）, complications and eye drop glaucoma medication were recorded at each follow-up visit. Success was defined as IOP reduction ≥20% from baseline. RESULTS： Forty-one eyes of 25 patients were included in this study. Pre-treatment mean IOP was 20.2±1.6 mm Hg. After PLT, IOP was 19.3±5.2, 16.1±2.7, 17.1±3.7 and 16.3±3.5 mm Hg,at 1 wk, 1, 3 and 6 mo, respectively. IOP reduction from baseline was statistically significant from the first month, remaining stable at 6 mo（P〈0.001）. PLT success at 6 mo of follow-up was 48.78%. The number of glaucoma medication per eye（P=0.10） and the mean BCVA both remained constant（P=0.37）. Complications included transient IOP spikes in 4 eyes（9.8%） and peripheral anterior synechiae in 7 eyes（17.1%）. CONCLUSION： PLT is an effective and safe method for the management of patients with OHT or OAG as an adjunctive therapy. Additional larger studies should be designed to verify the long-term stability of IOP reduction with this laser technology.

Srgap2 suppression ameliorates retinal ganglion cell degeneration in mice

Slit-Robo GTPase-activating protein 2(SRGAP2) plays important roles in axon guidance, neuronal migration, synapse formation, and nerve regeneration. However, the role of SRGAP2 in neuroretinal degenerative disease remains unclear. In this study, we found that SRGAP2 protein was first expressed in the retina of normal mice at the embryonic stage and was mainly located in the mature retinal ganglion cell layer and the inner nuclear layer. SRGAP2 protein in the retina and optic nerve increased after optic nerve crush. Then, we established a heterozygous knockout(Srgap2+/–) mouse model of optic nerve crush and found that Srgap2 suppression increased retinal ganglion cell survival, lowered intraocular pressure, inhibited glial cell activation, and partially restored retinal function. In vitro experiments showed that Srgap2 suppression activated the mammalian target of rapamycin signaling pathway. RNA sequencing results showed that the expression of small heat shock protein genes(Cryaa, Cryba4, and Crygs) related to optic nerve injury were upregulated in the retina of Srgap2+/– mice. These results suggest that Srgap2 suppression reduced the robust activation of glial cells, activated the mammalian target of rapamycin signaling pathway related to nerve protein, increased the expression of small heat shock protein genes, inhibited the degeneration of retinal ganglion cells, and partially restored optic nerve function.