Open AccessNuclear translocation of β-catenin induced by E-cadherin endocytosis causes recurrent erosion of diabetic cornea
Author(s) -
Wenbei Ma,
Zhengyuan Xie,
Hui Chen,
Lirong Zeng,
Xiaohong Chen,
Songfu Feng,
Xiaoyan Lu
Publication year - 2021
Publication title -
experimental biology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 146
eISSN - 1535-3702
pISSN - 1535-3699
DOI - 10.1177/1535370220983243
Subject(s) - endocytosis , corneal epithelium , catenin , cornea , cadherin , microbiology and biotechnology , epithelium , basement membrane , corneal ulceration , pathology , biology , chemistry , cancer research , cell , medicine , ophthalmology , biochemistry , wnt signaling pathway , signal transduction
Recurrent epithelial erosion and refractory corneal ulcer are the clinical features of diabetic keratopathy (DK), which eventually lead to corneal scar and visual disturbance. In this study, we sought to determine the abnormalities of cell junction in diabetic corneal epithelial cells and the effect of high glucose on the β-catenin/E-cadherin complex. Corneal histology showed that corneal epithelial cells of high glucose mice were loosely arranged, and the immunohistochemistry showed that the expression of E-cadherin decreased, the levels of β-catenin increased in nuclear. High glucose-induced degradation and endocytosis of E-cadherin of corneal epithelial cells reduce the formation of β-catenin/E-cadherin complex and promote the nuclear translocation of β-catenin. Moreover, high glucose also activated the transcription and expression of matrix metallopeptidase and snail, which interfered with the adhesion of corneal epithelial cells to the basement membrane. These findings reveal that DK is associated with the dissociation of cell junctions. The maintenance of the stability of the β-catenin/E-cadherin complex may be a potential therapeutic target of refractory corneal ulcers in patients with diabetes.