Rosiglitazone suppresses TGF-β1-induced myofibroblast activation and extra cellular matrix synthesis in pterygium fibroblasts at least partly through the modulation of the p38 MAPK pathway.
Rosiglitazone suppresses TGF-β1-induced myofibroblast activation and extra cellular matrix synthesis in pterygium fibroblasts at least partly through the modulation of the p38 MAPK pathway.
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.
15 specimens of pterygia from 15 eyes were examined, together with normal conjunctival tissue from the same eyes for the pattern of gene expression of genes associated with the induction or repression of apoptosis (p53, bcl-2, and bax).
This result was confirmed with double immunofluorescence labeling, revealing that in pterygium stromal TCs always showed a PDGFRα+/nestin+ and PDGFRα+/CD34+ immunophenotype.
Most significantly, western blotting confirmed that two candidate proteins matrix metalloproteinase 10 (MMP-10) and CD34 were significantly upregulated in pterygia, suggesting that they have potential roles in the pathogenesis of pterygia.
On the basis of biological processes in gene ontology, the identified proteins were mainly involved in cellular process, metabolic process, developmental process, location, cellular component organization, Among these proteins, matrix Metalloproteinase 10 (MMP-10) and CD34 may have potential roles in the pathogenesis of pterygia.
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.
The purpose of this study was to investigate hypermethylation of the p16 promoter in pterygia and the relationship between this hypermethylation and the expression of p16 and DNA methyltransferase 3b (DNMT3b) proteins.
The point missense mutations at codon 61 were glutamine to arginine (Glu61Arg CAA>CGA) in four cases and glutamine to leucine (Glu61Leu CAA>CTA) in three cases.ConclusionThe significantly higher frequency of codon 61 mutation of the ras oncogene in primary and bilateral pterygium specimens compared with normal conjunctiva supports the tumoral origin of pterygium, and thus set the stage for research into a targeted therapy for pterygium with better outcomes than surgical excision.