To compare refractive outcomes after cataract surgery between patients with closed-angle and open-angle glaucoma and evaluate the influence of preoperative factors on refractive outcomes in patients with glaucoma. Patients diagnosed with glaucoma and who underwent uncomplicated cataract surgery were enrolled in this retrospective observational study. We collected data including age, history of prior laser peripheral iridotomy and trabeculectomy, type of glaucoma, manifest refraction, intraocular pressure, axial length, and various anterior segment parameters using anterior-segment optical coherence tomography. Factors associated with unsatisfactory refractive outcome at postoperative 6 month were evaluated. A total of 143 eyes (143 subjects) were included. Of these, 49 and 94 had closed-angle and open-angle glaucoma, respectively. At postoperative-6 month evaluation, the mean absolute error (MAE) predicted by the SRK-II and SRK-T formulae was 0.67 ± 0.61 and 0.81 ± 0.66 diopters (D), respectively. The overall predictability of achieving within ± 1.0 D of target was 76.92 % and 72.73 %, respectively. At a cutoff value of 1.0 D for MAE, there was no statistical significant difference in refractive outcome between the closed-angle and open-angle glaucoma groups. Logistic regression modeling showed that large lens vault (LV) was a significant predictor of unsatisfactory refractive outcome after cataract surgery in patients with glaucoma. When considering cataract surgery in patients with glaucoma, surgeons should recognize that the refractive outcomes may be unsatisfactory in eyes with large LV.

The current study was undertaken to investigate whether histone deacetylases (HDACs) can modulate the viability of retinal ganglion cells (RGCs) and the activity of glial cells in a mouse model of retinal ischemia-reperfusion (IR) injury. C57BL/6J mice were subjected to constant elevation of intraocular pressure for 60 min to induce retinal IR injury. Expression of macroglial and microglial cell markers (GFAP and Iba1), hypoxia inducing factor (HIF)-1α, and histone acetylation was analyzed after IR injury. To investigate the role of HDACs in the activation of glial cells, overexpression of HDAC1 and HDAC2 isoforms was performed. To determine the effect of HDAC inhibition on RGC survival, trichostatin-A (TSA, 2.5 mg/kg) was injected intraperitoneally. After IR injury, retinal GFAP, Iba1, and HIF-1α were upregulated. Conversely, retinal histone acetylation was downregulated. Notably, adenoviral-induced overexpression of HDAC2 enhanced glial activation following IR injury, whereas overexpression of HDAC1 did not significantly affect glial activation. TSA treatment significantly increased RGC survival after IR injury. Our results suggest that increased activity of HDAC2 is closely related to glial activation in a mouse model of retinal IR injury and inhibition of HDACs by TSA showed neuroprotective potential in retinas with IR injuries.

Various neuroprotective agents have been studied for the treatment of retinal ganglion cell (RGC) diseases, but issues concerning the side effects of systemically administered drugs and the short retention time of intravitreally injected drugs limit their clinical applications. The current study aimed to evaluate the neuroprotective effects of intravitreally injected trichostatin A (TSA)-loaded liposomes in a mouse model of optic nerve crush (ONC) and determine whether TSA-loaded liposomes have therapeutic potential in RGC diseases. The histone deacetylase inhibitor, TSA, was incorporated into polyethylene glycolylated liposomes. C57BL/6J mice were treated with an intravitreal injection of TSA-loaded liposomes and liposomes loaded with a lipophilic fluorescent dye for tracking, immediately after ONC injury. The expression of macroglial and microglial cell markers (glial fibrillary acidic protein and ionized calcium binding adaptor molecule-1), RGC survival, and apoptosis were assessed. We found that the liposomes reached the inner retina. Their fluorescence was detected for up to 10 days after the intravitreal injection, with peak intensity at 3 days postinjection. Intravitreally administered TSA-loaded liposomes significantly decreased reactive gliosis and RGC apoptosis and increased RGC survival in a mouse model of ONC. Our results suggest that TSA-loaded liposomes may help in the treatment of various RGC diseases.

Background: To investigate long-term outcomes of prediction error after phacotrabeculectomy and to determine risk factors that may cause unstable prediction error after phacotrabeculectomy in glaucoma patients. Methods: A total 120 eyes of 120 patients who had underwent uncomplicated phacotrabeculectomy (combined group) or phacoemulsification (phaco-only group) were included. Best-corrected visual acuity (BCVA), intraocular pressure (IOP) were measured before and after surgery, and anterior segment parameters including anterior chamber depth (ACD), lens vault (LV), and anterior vault (AV) measured using anterior-segment optical coherence tomography were compared between the two groups. The mean absolute error (MAE) at 3, 6, 12, and 24 months postoperatively were compared. Risk factors associated with unstable prediction error (MAE ≥ 0.5) were investigated in the combined group. Results: In both groups, BCVA was improved and IOP was decreased significantly. MAE at 3, 6, 12, 24 months postoperatively were not significantly different between two groups. The risk factors for unstable prediction error after 12 months of phacotrabeculectomy were old age and LV. Whereas, the only factor predicting unstable prediction error after 24 months of phacotrabeculectomy was LV. The cut-off value of LV for predicting unstable refractive error analyzed by the ROC curve was 0.855 mm. Conclusions: Phacotrabeculectomy may be an effective treatment with stable long-term outcomes of prediction error similar to phacoemulsification in patients with glaucoma. However, elderly patients or patients with large LV may be predisposed to unstable prediction error after phacotrabeculectomy.

We aimed to investigate the effects of different concentrations of vascular endothelial growth factor (VEGF) on the extracellular matrix (ECM) and fibrotic proteins in human trabecular meshwork (TM) cells. We also explored how the Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) signaling pathway modulates VEGF-induced fibrosis. We determined cross-linked actin network (CLAN) formation using TM cells. Changes in fibrotic and ECM protein expression were determined. High VEGF concentrations (10 and 30 ng/mL) increased TAZ and decreased p-TAZ/TAZ expression in TM cells. Western blotting and real-time PCR revealed no YAP expression changes. Fibrotic and ECM protein expression decreased at low VEGF concentrations (1 and 10 ρg/mL) and significantly increased at high VEGF concentrations (10 and 30 ng/mL). CLAN formation increased in TM cells treated with high VEGF concentrations. Moreover, TAZ inhibition by verteporfin (1 μM) rescued TM cells from high-VEGF-concentration-induced fibrosis. Low VEGF concentrations reduced fibrotic changes, whereas high VEGF concentrations accelerated fibrosis and CLAN formations in TM cells in a TAZ-dependent manner. These findings reflect the dose-dependent influences of VEGF on TM cells. Moreover, TAZ inhibition might be a therapeutic target for VEGF-induced TM dysfunction.