Abstract
Purpose :
Although the phenotype of pterygium has known as high levels of proliferation, inflammation, angiogenesis, and extensive amount of extracellular matrix accumulation, the specific molecular mechanism of pterygium pathogenesis is still unclear. Here, we aim to understand the underlying molecular mechanism of pterygium pathogenesis.
Methods :
Transcriptome analyses using human pterygium epithelial cells and fibroblasts isolated from primary pterygium tissue. Quantitative polymerase chain reaction (PCR) and wound scratch test were performed to compare characteristics between pterygial and normal conjunctival cells. Traction force microscope (TFM) analysis and migration ability in different matrix stiffness conditions (matrix stiffnesses to mimic normal (~2.5 kPa) and pterygial (~60 kPa) tissue) were compared between pterygial and normal conjunctival cells.
Results :
Cell adhesion and migration-associated signaling pathways were significantly upregulated in the pterygium epithelial cells and fibroblasts compared to cells isolated from normal conjunctival tissue, which were validated by quantitative PCR (matrix metalloproteinase, integrin alpha) and wound scratch assays. TFM analyses revealed that pterygium cells showed significantly higher levels of mechano-sensitiveness to their microenvironment and underwent mechanotransduction. Cells cultured on a stiff matrix exhibited increased growth, elongation, and numbers of vinculin, and furthermore, the same cell behaviors were significantly increased in both pterygium-derived cells, compared to cells on soft matrix.
Conclusions :
These findings may offer insight into the important roles of cell-matrix interactions in pterygium pathophysiology, which could provide a valid tool to develop potential therapeutic candidates.
This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.