Evaluation of Mooren's corneal ulcer by anterior segment optical coherence tomography.

BACKGROUND: This study evaluates the use of anterior segment optical coherence tomography (AS-OCT) to identify focal changes and inform surgical plans in eyes with Mooren's ulcer. METHODS: A total of 18 eyes of 17 patients with Mooren's ulcer were examined prospectively using the AS-OCT system. RESULTS: Optical hyperreflectivity noted on AS-OCT images was in accordance with corneal ulceration, neovascularization, fibrovascular membranes, the junction of the native stromal bed, and the overlying lamellar corneal grafts. Focal corneal ectasia was observed in 13 eyes with a decrease in corneal thickness to ≤0.39 mm. There was a cut-off value of 0.39 mm in corneal thickness between the eyes with and without focal corneal ectasia in the thinned corneal area (Fisher = 0.383, χ2 = 14.873, P = 0.000). Based on the AS-OCT findings, six eyes were subjected to an individualized lamellar corneal graft. The thickness of the residual cornea after surgery was 47 ± 34 µm less than the presumed healthy corneal thickness before surgery (t = 3.376, P = 0.02). A small corneal perforation covered by a pseudopterygium in Mooren's ulcer was found through AS-OCT but undetectable by slit-lamp biomicroscopy. CONCLUSIONS: AS-OCT is a valuable non-contact technique for monitoring corneal thinning in Mooren's ulcer, and assisting surgical design. A decrease in peripheral corneal thickness to ≤0.39 mm may cause focal corneal ectasia.

Therapeutic effects of a novel venom abstract (ZK002) solution in an alkali-burned corneal wound-healing model.

Purpose: Corneal alkali burns can progress to corneal epithelial defects, inflammation, scarring, and angiogenesis, potentially leading to blindness. Therefore, we examined the therapeutic effects of a novel ophthalmic solution (ZK002) on wound healing in alkali-burned rat corneas. Methods: In this study, we attempted to treat alkali-exposed rat corneas using topical application of either an ophthalmic solution with ZK002 or an anti-vascular endothelial growth factor agent for 14 days. We evaluated corneal edema, corneal neovascularization area, and histological changes. We also assessed the inflammatory (MMP-9, MMP-2, and interleukin-1ß) and angiogenic (vascular endothelial growth factor receptor 2, VEGFR2) markers. Levels of inflammatory (matrix metalloproteinase (MMP)-9, MMP-2, and interleukin-1ß), profibrotic (α-smooth muscle actin, α-SMA; transforming growth factor-ß2,TGF-ß2), and angiogenic (vascular endothelial growth factor-receptor 2, VEGFR2) factors, as well as peroxisome proliferator-activated receptor γ (PPARγ) mRNA expression, were measured. Results: The analyses showed that alkali exposure caused an increase in corneal edema and fibrosis with corneal neovascularization. The accumulation of α-smooth muscle actin-positive myofibroblasts and the deposition of transforming growth factor-ß2 on the alkali-exposed corneas were noted on day 14. The mRNA expression levels of interleukin-1ß, MMP-9, MMP-2, VEGFR2, and profibrotic factors were decreased in the ZK002 group compared with the control group during the early period of corneal alkali burns on day 14. However, the expression level of PPARγ mRNA was increased in the ZK002 group. Conclusions: ZK002 decreased the fibrotic reaction and prevented neovascularization in the cornea after an alkali burn. Therefore, the novel ophthalmic solution ZK002 could be a potentially promising therapeutic clinical treatment for corneal wound healing.

Effects of PPAR-γ and RXR-α on mouse meibomian gland epithelial cells during inflammation induced by latanoprost.

The purpose of this study is to investigate the effects of latanoprost on the secretion of cytokines and chemokines from meibomian gland epithelial cells, and to evaluate the modulation of peroxisome proliferator-activated receptor γ (PPAR-γ) and retinoid X receptor α (RXR-α) during latanoprost-induced inflammation. Mouse meibomian gland epithelial cells were cultured in proliferation and differentiation medium, respectively. Cells were exposed to latanoprost, rosiglitazone (PPAR-γ agonist), or LG100268 (RXR-α agonist), respectively. The expression of IL-6, IL-1ß, TNF-α, MMP-9, MCP-1, and CCL-5 were detected by real-time PCR and ELISA. The effect of latanoprost, rosiglitazone, LG100268, and inflammatory cytokines on the differentiation of meibocyte were evaluated by related gene expression and lipid staining. The expression of Keratin-1, 6, 17 protein was detected by western immunoblotting. The results showed that the above cytokines could be induced by latanoprost in meibomian gland epithelial cells. LG100268 and rosiglitazone could inhibit the production of IL-6 and TNF-α induced by latanoprost, respectively. Latanoprost suppressed the expression of differentiation-related mRNA through a positive feedback loop by enhancement of COX-2 expression via FP receptor-activated ERK signaling. The expression of Keratin-17 was upregulated by rosiglitazone and suppressed by LG100268. The application of IL-6 and TNF-α showed negative effects on lipid accumulation in meibomian gland epithelial cells. These results demonstrated that latanoprost could induce inflammation and suppress differentiation of mouse meibomian gland epithelial cells. The activation of PPAR-γ and RXR-α showed an anti-inflammatory effect, showing a potential role to antagonize the effect of latanoprost eyedrops on meibomian gland epithelial cells.