LOXL1 expression in lens capsule tissue specimens from individuals with pseudoexfoliation syndrome and glaucoma.

PURPOSE: To study lysyl oxidase-like 1 (LOXL1) expression in freshly collected lens capsules from pseudoexfoliation syndrome (XFS), pseudoexfoliation glaucoma (XFG), and normal cataract control individuals. We also investigated the effects of four glaucoma drug medications on LOXL1 expression in primary human lens epithelial cell cultures to see if they could affect LOXL1 expression. METHODS: Lens capsules were collected at the time of cataract surgery. Controls were matched to age, sex, and ethnicity. Total RNA was isolated from individual lens capsule samples and real-time PCR was performed on each sample using primers flanking the sixth exon of the LOXL1 gene. Cell cultures were grown to confluence in four separate six-well plates at 37 °C in 5% CO2. Each plate was then treated with one of four different glaucoma drugs (brinzolamide 1%, brimonidine tartrate 0.1%, timolol maleate 0.5%, and latanoprost 0.005%) once daily for seven days (at both 1:1,000 and 1:100 concentrations relative to media). Controls were not treated with any drug but media was changed in the same manner. After one week of treatment, cells were harvested and total RNA isolated. Real-time PCR was performed on each group of cells. RESULTS: Seven XFS, seven XFG, and ten cataract control specimens were analyzed. LOXL1 expression was detected in the lens capsule specimens from each of the four groups. Significant expression differences were found between the control and XFG groups and XFS and XFG groups. No significant difference was observed between the control and XFS group. No significant decrease in LOXL1 expression was seen with drug incubation of the four medications (Brinzolamide, Timolol, Latanoprost, and Brimonidine) at the 1:1,000 drug:media concentrations versus controls. At 10-fold higher concentrations (1:100 drug:media), brinzolamide, timolol maleate, and latanoprost showed small increases in LOXL1 expression relative to controls. This effect was not observed with brimonidine tartrate. CONCLUSIONS: These results establish that LOXL1 expression is reduced in lens capsule specimens from XFG individuals but not XFS. The drug treatment incubation studies suggest that the change in LOXL1 expression observed in XFG is not attributable to glaucoma drug therapy. If a causative functional relationship can be validated, modification of LOXL1 expression in affected tissues may represent a novel treatment strategy for this disorder.

Age and racial variation in central corneal thickness of preschool and school-aged children.

PURPOSE: The purpose of this study was to determine variations in central corneal thickness (CCT) of preschool and school-aged African American and white children. Secondary aims were to assess possible correlations between CCT measurements and gender, axial length, intraocular pressure (IOP), family history of glaucoma, or history of prematurity. METHODS: Contact ultrasound was used to measure CCT and axial length in 76 white and 60 African American children between the ages of 7 months and 18 years. A questionnaire was completed by the parents or guardians, including medical and family history. Statistically significant associations and differences were assessed using the independent t test, analysis of variance, and linear regression. All associations were defined as significant when the alpha value was less than 0.05 (two-tailed). RESULTS: Mean CCT was thinner in African American children (535 +/- 35 microm) compared to white children (559 +/- 38 microm) (P < .001). The corneal thickness in children ages 10 to 18 years was significantly higher than in all other age groups in both African American (P = .03) and white (P < .005) children. No association was found between CCT and gender, axial length, IOP, or family history of glaucoma. Premature children had thinner CCT (536 +/- 40 pm) than full-term children (552 +/- 38 microm) (P = .009). CONCLUSIONS: African American children have a thinner CCT compared to white children at all ages. Children of both racial groups have an increasing value of CCT with increasing age after approximately age 10 years. Children born prematurely have a thinner CCT than full-term children.