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We evaluated the changes in substance P (SP)-expressing trigeminal neurons (TNs) innervating the cornea following ocular surface inflammation. Ocular surface inflammation was induced in Sprague–Dawley rats using 0.1% benzalkonium chloride (BAK). The corneal staining score, corneal epithelial apoptosis, conjunctival goblet cells, and density of corneal subbasal nerve plexus (SNP) were assessed, and the mRNA levels of SP, interleukin (IL)-1β, IL-6, and tumour necrosis factor-α were measured in corneas and ipsilateral trigeminal ganglia (TG). SP-immunoreactivity (IR) was measured in corneal intraepithelial nerves and TNs. The cell size of corneal TNs in the TG was calculated. All parameters were observed immediately (BAK group), at 1 week (1 w group), and 2 months (2 m group) after 2 weeks of BAK application. BAK caused an increase in the corneal staining score and the number of apoptotic cells, loss of conjunctival goblet cells, reduced density of corneal SNP, and upregulated expression of SP and inflammatory cytokines in both the cornea and TG in the BAK group but those changes were not observed in the 2 m group. On the other hand, SP-IR% and mean cell size of corneal TNs increased significantly in the BAK, 1 w, and 2 m groups, compared to the control. Our data suggest that following ocular surface inflammation, large-sized corneal TNs which normally do not express SP, expressed it and this phenotype switching lasted even after the inflammation disappeared. Long-lasting phenotypic switch, as well as changes in the expression level of certain molecules should be addressed in future studies on the mechanism of corneal neuropathic pain.

Glaucoma is one of the irreversible ocular diseases that can cause vision loss in some serious cases. Although Triggerfish has been commercialized for monitoring intraocular pressure in glaucoma, there is no smart contact lens to monitor intraocular pressure and take appropriate drug treatment in response to the intraocular pressure levels. Here, we report a precisely integrated theranostic smart contact lens with a sensitive gold hollow nanowire based intraocular pressure sensor, a flexible drug delivery system, wireless power and communication systems and an application specific integrated circuit chip for both monitoring and control of intraocular pressure in glaucoma. The gold hollow nanowire based intraocular pressure sensor shows high ocular strain sensitivity, chemical stability and biocompatibility. Furthermore, the flexible drug delivery system can be used for on-demand delivery of timolol for intraocular pressure control. Taken together, the intraocular pressure levels can be successfully monitored and controlled by the theranostic smart contact lens in glaucoma induced rabbits. This theranostic smart contact lens would be harnessed as a futuristic personal healthcare platform for glaucoma and other ocular diseases. Glaucoma is an irreversible ocular disease that may lead to vision loss. Here the authors develop a theranostic smart contact lens with an intraocular pressure sensor, a flexible drug delivery system, wireless power and communication systems and an application specific integrated circuit chip for both monitoring and control of intraocular pressure in glaucoma induced rabbits.

Keratoconus is a bilateral ectatic disorder characterized by the central thinning of corneal tissue leading to visual impairment. To investigate the possibility of visual system homeobox 1 ( VSXI) as a candidate susceptibility gene for Korean patients with keratoconus, we performed a mutation screening of the VSXI gene in 249 unrelated patients with keratoconus and 208 control subjects without the ocular disorder. We found two heterozygous novel missense mutations in exon 2: N151S and G160V. The G160V mutation was identified in 13 keratoconus patients (5.3%), and the N151S mutation was found in only one keratoconus patient (0.4%). We also detected three synonymous polymorphisms and four intragenic polymorphisms. The IVS1-11*a allele was associated with a significantly increased risk of keratoconus in Korean patients [3.6 vs. 0.5%, p  = 0.001, odds ratio (OR) = 7.76, 95% confidence interval (CI) 1.989–30.241). Other polymorphisms did not show an association with keratoconus risk. Our data is the first reported VSX1 mutation screening in Korean keratoconus patients. We detected two novel missense mutations and one intragenic polymorphism in the VSX1 gene, which show a strong statistical association with unrelated keratoconus patients. Consequently, our study suggests that VSX1 gene variants seem to be significant genetic variants for keratoconus predisposition in unrelated Korean patients.

Diabetic retinopathy is currently treated by highly invasive repeated therapeutic injections and surgical interventions without complete vision recovery. Here, a noninvasive smart wireless far red/near‐infrared (NIR) light emitting contact lens developed successfully for the repeated treatment of diabetic retinopathy with significantly improved compliance. A far red/NIR light emitting diode (LED) is connected with an application‐specific integrated circuit chip, wireless power, and communication systems on a PET film, which is embedded in a silicone elastomer contact lens by thermal crosslinking. After in vitro characterization, it is confirmed that the retinal vascular hyper‐permeability induced by diabetic retinopathy in rabbits is reduced to a statistically significant level by simply repeated wearing of smart far red/NIR LED contact lens for 8 weeks with 120 µW light irradiation for 15 min thrice a week. Histological analysis exhibits the safety and feasibility of LED contact lenses for treating diabetic retinopathy. This platform technology for smart LED contact lens would be harnessed for various biomedical photonic applications. A noninvasive smart wireless far red/near‐infrared (NIR) light emitting contact lens is developed for the repeated treatment of diabetic retinopathy. The diabetic retinopathy in rabbits is reduced to a statistically significant level by simple repeated wearing of smart far red/NIR light emitting diode contact lens for 8 weeks with 120 µW light irradiation for 15 min thrice a week.

To determine the effect of hyperosmolarity on cell survival/apoptosis of conjunctival epithelial cells and evaluate the possible role of IL6, Wong-Kilbourne derivative of Chang conjunctival cell line (WKD) was used in this study. Confluent cells were incubated under different osmolarity (290 mOsm and 500 mOsm) with or without neutralizing IL6 antibody (50 ng/mL). The expression of IL6 level was measured in the supernatant of each conditioned medium. Cell viability/apoptosis assay was performed using Annexin V/Propidium Iodide (PI) and Cell Counting Kit-8 (CCK-8). Western blot was conducted to measure the abundance of apoptotic markers and IL6 related downstream signaling pathway. The concentration of IL6 showed time-dependent increase in cells treated with 500 mOsm. Although apoptosis of WKD cell is increased in treated 500 mOsm for 24 h, apoptosis reduced in WKD cell treated 500 mOsm with anti-IL6 for 24 h. Anti-IL6 inhibited the activation of JAK-STAT signaling pathway, which was induced by hyperosmolarity. Hyperosmolar condition induced apoptosis in conjunctival epithelial cells, along with increase of IL6 production. IL6 neutralizing antibody inhibited apoptosis and JAK-STAT signaling in hyperosmolar condition. These findings suggested that IL6 may be involved in apoptotic change and in hyperosmolarity.

To investigate the potential risk factors associated with nuclear, cortical, posterior subcapsular, and anterior polar cataracts (APC) in the Korean population. This was a population-based, cross-sectional study of 7992 adults (over 40 years of age) from the data of the fourth annual Korea National Health and Nutrition Examination Survey, performed from 2007 to 2009. The presence of lens opacity was examined by slit-lamp biomicroscopy and evaluated according to LOCS II standard photographs. The subtype of cataract present, including nuclear, cortical, posterior subcapsular, and anterior polar cataracts, was noted. Multivariable adjusted logistic regression analysis was conducted to examine the odds ratio (OR) and 95% confidence interval (CI) for association of each specific type of cataract with age, sex, health examination, and medical history. The prevalence of nuclear, cortical, and posterior subcapsular cataract increased gradually with increasing age. However, the prevalence of APC peaked in the 50- to 59-year-old subjects. All types of cataract except for APCs were more prevalent in women. Oral steroid use was associated with a lower risk of APC. These findings showed the unique characteristics of APC in the Korean population.

Purpose: The purpose of this study was to establish a simple, xeno-feeder-free method for cultivating human corneal epithelial cells. Methods: Limbal tissue explants from a cadaver were cultured in Iscove's modified Dulbecco's medium and low-calcium Panserin 801 medium in a 1:1 ratio. The outgrowing cells were characterized by flow cytometry, immunohistochemistry and real-time PCR (rtPCR). Limbal epithelial cells were expanded in a xeno-feeder-free, low-calcium medium and airlifted for 2 weeks each. Results: Migration of fibroblast-like stromal cells initially occurred from the limbal explants, and then epithelial cells migrated and grew on the stromal cells as an autofeeder layer. After airlifting, the cultured epithelium consisted of two to three layers. The cultured cells expressed stem cell-associated markers (ABCG2 and ΔNp63), differentiation markers (CK3 and CK12) and extracellular matrix-associated markers (lumican and decorin). rtPCR showed increased expression of markers for epithelial progenitor cells compared to fresh limbal tissue. Side population cells comprised 0.43 ± 0.04% of the cells (n = 5) in the primary culture. Flow cytometry showed that 49.12, 40.44 and 44.55% of the cells from the explants expressed E-cadherin, ΔNp63 and ABCG2, respectively. Conclusion: This explant culture system using stromal cells as an autofeeder layer was useful in expanding human corneal epithelial cells. This system may offer clinical insight for the expansion of limbal progenitor cells for the reconstruction of the ocular surface.

Although the mechanism of dry eye disease is not clearly understood, it is certain that inflammation and the immune response play a major role in determining the health of the ocular surface in dry eye patients. Accurate ocular surface characterization during the early stages of dry eye disease is critical for successful treatment, because there exists no single standard, objective test to diagnose the early phase of dry eye disease. The treatment target should be direct to prevent the perpetuation of chronic inflammation and immune responses. Numerous studies have categorized dry eye disease as an autoimmune-related inflammatory disease. However, relatively little is known about how innate immune mechanisms act following a local insult, why some patients are particularly vulnerable, and why local inflammation fails to resolve in these patients. Within this review, particular attention will be given to the very early events and corresponding defense mechanism in dry eye disease. The transition from innate to adaptive immunity will also be discussed.

Corneal dystrophies (CDs) are a diverse group of inherited disorders with a heterogeneous genetic background. Here, we report the identification of a novel ZNF143 heterozygous missense mutation in three individuals of the same family with clinical and pathological features that are consistent with endothelial CD. Ophthalmologic examination revealed diffuse corneal clouding and edema with decreased endothelial cell density. Pathological findings showed increased corneal thickness due to edema of basal epithelial cells and stroma, and abnormal metaplastic endothelium with stratified epithelium-like changes. Patients’ metaplastic corneal endothelial cells expressed predominantly cytokerain 7, cytokeratin 19, and E-cadherin. Although Sanger sequencing did not detect any mutation associated with endothelial CDs, whole exome sequencing identified the ZNF143 c.937G>C p.(Asp313His) mutation as a candidate gene for our patients’ endothelial CD. In-vitro functional studies demonstrated that mutant ZNF143 promoted the mesenchymal-to-epithelial transition; it upregulated the expression of genes associated with epithelialization in human corneal endothelial cells. Additionally, proinflammatory cytokine responsive genes were significantly enriched after mutant ZNF143 transfection, which may contribute to the severe phenotype of the three patients. These findings link a mutation in ZNF143 with endothelial CD for the first time.