Tear film levels of interleukin- (IL-) 6, IL-8, and vascular endothelial growth factor (VEGF) were investigated over time, and preoperative concentrations were linked to corneal neovascularization and pterygium size.
IL-6 and -8 proteins were abundantly expressed, predominantly by the pterygium epithelium, with additional IL-8 immunoreactivity associated with the vascular endothelium.
S100A8 and S100A9 were localized in the superficial layer of both pterygium and normal conjunctiva epithelium, with higher levels in pterygium than uninvolved conjunctiva.
This study indicates that pterygium and pinguecula have an altered metabolism of cholesterol-namely increased LDL-R and HMG-CoA-R mRNAs-as is characteristic of tumorlike tissues, and that the high expression of LDL receptors renders them amenable to be treated by photodynamic therapy with intravenously injected verteporfin.
We found that after exposure to VEGF, mRNA and protein levels of LDLr were both increased significantly in PSFs, assessed using relative quantitative real-time RT-PCR and Western blot.
We propose here a series of intracellular events where CRIM1 regulation of the ERK pathway prevents UV-induced cell proliferation and may play an important role in the in the pathogenesis of pterygium.
Because the polymorphism of hOGG1 was reported to be associated with pterygium, it is logical to assume the correlation between XRCC1, XPA, and XPD polymorphisms and pterygium formation.
Concurrently used MBS item numbers 42 686 (pterygium removal) with 42 641 (conjunctival autograft) and also 42 686 with any other ophthalmic item number.
UVA irradiation increased the uPA mRNA levels in pterygium fibroblasts and the uPA activities in cultured medium, which was accompanied with an increase in phosphorylated ERK and JNK.
Pterygium cell line (PECs) cell models were used to confirm the effect of β-catenin, miR-221, and p27Kip1 gene in the proliferation of pterygium cells.
Overexpression of MMP-1 and MMP-3, a phenotype previously linked with UV exposure in dermal fibroblasts to explain the pathologic finding of elastotic degeneration, suggests that pterygium head fibroblasts might be intrinsically altered by UV, which might be responsible for corneal invasion.
Here we investigated the role of IPO13 in the pathogenesis of pterygium and the underlying mechanism including interaction with other cell proliferation-related factors: keratin 17 (K17), a lesional protein and a member of the type I keratins, and c-Jun, a protein of the activator protein-1 complex.
The expression of PSMB5 and Nrf2 by pterygium fibroblasts was suppressed in a dose dependent manner following UVB radiation of 0-50 mJ/cm<sup>2</sup> doses.