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.
A gene signature consisting of 11 DEGs were found to be shared by pterygium and MGD (SPRR3, SERPINB13, NMU, KRT10, IL37, KRT6B, PI3, S100A2, MAL, AURKA, and RGCC), and bioinformatics analyses showed that these overlapped DEGs were significantly enriched in pathways related to keratinization, cell-cycle regulation, and formation of the cornified envelope.
Abnormal p53 expression in the epithelium of primary and recurrent pterygium specimens suggests that pterygium is a growth disorder rather than a degeneration.
After p53 protein was found to be abnormally expressed in the epithelium, researchers suggested that a pterygium may be a tumor, but additional evidence is required to support this hypothesis.
Although, these results suggest that overexpression of peroxiredoxin 2 in pterygium could protect the cell against oxidative stress-induced apoptosis, further studies are required to establish the functional role of peroxiredoxin 2 in pterygium to determine its role in peroxidation and apoptosis in this pathology.
Among these genes, we chose three proteins, aldehyde dehydrogenase, dimeric NADP-preferring (ALDH3A1), protein disulfide-isomerase A3 (PDIA3), and peroxiredoxin-2 (PRDX2), that were significantly upregulated in pterygium and further increased in recurrent pterygium.
Among these genes, we chose three proteins, aldehyde dehydrogenase, dimeric NADP-preferring (ALDH3A1), protein disulfide-isomerase A3 (PDIA3), and peroxiredoxin-2 (PRDX2), that were significantly upregulated in pterygium and further increased in recurrent pterygium.
An expression of RAD50 gene in the conjunctiva originating from eyes with pterygium in comparison to the conjunctiva of control group was shown to be considerably higher.
Antibodies raised against VEGF and p53 were used to analyze the distribution and expression of these markers in pterygium and normal human conjunctiva were used as negative control.
Because pterygium is an UV-related uncontrolled cell proliferation, it is logical to assume polymorphisms of Ku70 is associated with genetic predisposition to 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.