TLR3 Gene Regulates Cataract-Related Mechanisms Through The Jagged-1/Notch Signaling Pathway

Abstract Objective: Epithelial-mesenchymal transition (EMT) is the main cause of organ fibrosis and a common pathogenesis of most cataracts. Therefore, TLR3 may play a vital role in the progress of PCO EMT. This study aims to explore the molecular mechanism of TLR3 in the occurrence and development of post-cataract EMT, and to provide new ideas for the prevention and treatment of posterior capsule opacification (PCO).Materials and Methods: The expression of TLR3 and EMT-related factors in samples from normal and PCO patients was measured by qPCR. In the presence or absence of TLR3, human lens epithelial cell line SRA01/04 are treated with TGF-β2. The CCK-8 method measures cell proliferation, and the Transwell method detects migration and invasion. The expression of EMT-related molecules and Jagged-1/Notch signaling pathway was analyzed by Western blot and qPC experiments.Result: In terms of mechanism, the functional gain and loss experiments of human LEC show that TLR3 regulates the proliferation, migration, invasion of LEC and EMT induced by TGF-β2 by targeting the Jagged-1/Notch signaling pathway to affect the development of fibrotic cataract.Conclusion: These findings indicate that TLR3 prevents the progression of lens fibrosis by targeting the Jagged-1/Notch signaling pathway to regulate LEC proliferation, migration, invasion and TGF-β2-induced EMT. "TLR3-Jagged-1/Notch" signal axis may be a therapeutic target for the treatment of fibrotic cataract.