| Summary: | 博士 === 中山醫學大學 === 醫學研究所 === 99 === Pterygium is a common ocular surface disease. It is a fibrovascular tissue which originate near the corneal-conjunctival junction and centripetally to encroach on the normal cornea. More and more researchers consider that pterygium is a tumor rather than degenerative disease. The migration and invasion of tumor cells correlate with the interaction between MMPs and TIMPs. Matrix metalloproteinases (MMPs) are a family of neutral proteolytic enzymes capable of denaturing most components of the extracellular matrix. They are grouped according to their substrate specificity. According to the composed collagen type of cornea, MMP-9 and MMP-10 were assumed to involve the invasion and migration mechanism in pterygium. At the level of inhibition, where MMPs are regulated by their specific tissue inhibitors (TIMPs). Therefore, MMP-9, MMP-10, and TIMP-1 proteins were studied using immunohistochemistry on 82 pterygial specimens and 30 normal conjunctivas. Among the 82 pterygial samples, 29 specimens (35.4%) were positive for MMP-9 expression, 28 were positive for MMP-10 (34.1%), and 59 were positive for TIMP-1 (72.0%). Staining for MMPs was limited to the cytoplasm of the epithelial layer. The TIMP-1 staining was detected in the pterygium epithelium, fibroblasts and corneal epithelium.
For further investigate if the invasion ability change after inhibiting TIMPs, pterygium epithelial cells (PECs) were cultured in a serum-free culture medium, and siRNA were used to knock down TIMP gene expression to evaluate the differential ability of pterygium invasion. In the cell model, cell invasion and migration ability increased in TIMP-1 knockdown PECs compared with the parental control. In conclusion, MMP-9 and MMP-10 may each play a role in pterygium formation, and TIMP-1 may contribute to pterygium invasion inhibition.
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