Abnormal p53 expression in the epithelium of primary and recurrent pterygium specimens suggests that pterygium is a growth disorder rather than a degeneration.
Fluorescence telomeric repeat amplification protocol was used to measure telomerase activity in whole pterygium samples from 9 cases and in the epithelium and stroma of pterygium from another 10 cases. p53 protein content was measured by enzyme-linked immunosorbent assay (ELISA) in tissues obtained from 7 eyes, as well as in epithelial cell suspensions collected by brush cytology in 8 eyes.
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.
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.
IL-6 and -8 proteins were abundantly expressed, predominantly by the pterygium epithelium, with additional IL-8 immunoreactivity associated with the vascular endothelium.
The increased expression of IGFBP-2 mRNA and protein in pterygium fibroblasts is further strong evidence to support the transformed phenotype of these cells and helps explain why there is increased growth of fibrovascular tissue.
A dose- and time-dependent increase in MMP-1 was observed when pterygium epithelial cells were exposed to UVB with no significant modulation of inhibitor activity.
We have analyzed the status and expression of the p53 gene in epithelial cells derived from pterygium and have demonstrated that the p53 gene has undergone a monoallelic deletion.
The correlation between pterygium and TNF-alpha-308 promoter, IL-1beta-511 promoter, IL-1beta exon 5, and IL-1 Ra polymorphisms does not exist and those polymorphisms are not useful genetic markers for pterygium susceptibility.
The correlation between pterygium and TNF-alpha-308 promoter, IL-1beta-511 promoter, IL-1beta exon 5, and IL-1 Ra polymorphisms does not exist and those polymorphisms are not useful genetic markers for pterygium susceptibility.
The correlation between pterygium and TNF-alpha-308 promoter, IL-1beta-511 promoter, IL-1beta exon 5, and IL-1 Ra polymorphisms does not exist and those polymorphisms are not useful genetic markers for pterygium susceptibility.
Three of them--namely T-box transcription factor-22 (TBX22), poliovirus receptor like-1 (PVRL1), and interferon regulatory factor-6 (IRF6)--are responsible for causing X-linked cleft palate, cleft lip/palate-ectodermal dysplasia syndrome, and Van der Woude's and popliteal pterygium syndromes, respectively; they are also implied in non-syndromic cleft lip and palate.