Nuclear translocation of β-catenin induced by E-cadherin endocytosis causes recurrent erosion of diabetic cornea.

摘要: Recurrent epithelial erosion and refractory corneal ulcer are the clinical features of diabetic keratopathy (DK), which eventually lead to scar visual disturbance. In this study, we sought determine abnormalities cell junction in cells effect high glucose on β-catenin/E-cadherin complex. Corneal histology showed that mice were loosely arranged, immunohistochemistry expression E-cadherin decreased, levels β-catenin increased nuclear. High glucose-induced degradation endocytosis reduce formation complex promote nuclear translocation β-catenin. Moreover, also activated transcription matrix metallopeptidase snail, interfered with adhesion basement membrane. These findings reveal DK is associated dissociation junctions. The maintenance stability may be a potential therapeutic target ulcers patients diabetes.