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Abstract
Glaucoma is one of the leading causes of blind worldwide. Post-operative scar formation of filtering tract was one of the main reasons for failure of glaucoma filtration surgery. In this study, we conducted several experiments to detect the expression of miR-26a in the scar tissue in filtering tract and then detect its potential biological effects as well as its target gene. In our present study, it was found that miR-26a was significantly down-regulated in filtering tract scar. Advanced study on the association between the miR-26a and connective tissue growth factor (CTGF) micro RNA (mRNA) showed that miR-26a was inversely correlated with CTGF mRNA level. Advanced biological studies showed that overexpression of miR-26a could decrease the cell viability and migration ability of human Tenon’s fibroblasts (HTFs) fibrosis in vitro model. It was also found that miR-26a might up-regulate the apoptotic level of HTFs. Through protein expression detection and luciferase reporter assay, it was found that miR-26a could produce functions that directly target the CTGF. In conclusion, the key finding of the current study is that miR-26a can suppress the activation of HTFs by transforming growth factor (TGF)-β by targeting CTGF. This data indicates that miR-26a plays an essential role in the formation of filtering tract scar and function as a potential drug target.
Acknowledgements
None.
Disclosure statement
The authors declare no conflict of interest.