Activation of autophagy inhibits epithelial to mesenchymal transition process of human lens epithelial cells induced by high glucose conditions.

Activation of autophagy inhibits epithelial to mesenchymal transition process of human lens epithelial cells induced by high glucose conditions. Cell Signal. 2020 Sep 04;:109768 Authors: Li J, Ye W, Xu W, Chang T, Zhang L, Ma J, Pei R, He M, Zhou J Abstract Subcapsular cataracts are common phenotype of diabetic cataracts, and abnormal lens epithelial cells (LECs) under the lens capsules have been considered to involve in the pathogenesis. Our previous studies have shown that the epithelial to mesenchymal transition (EMT), which is responsible for the LECs to lose their original polarity and tight junctions, occurs in a diabetic cataract mouse model. Autophagy is known to function in the EMT process in multiple tissues. However, the relationship between autophagy and EMT process in LECs has not yet been fully demonstrated. We found that high glucose retreatment reducing expression level of E-cadherin, an epithelial marker, but increasing that of α-smooth muscle actin (α-SMA), a mesenchymal marker, by Western blot and immunoflurence staining assays, and increased the cell migration by Transwell assay in human lens epithelial cell line HLE-B3. High glucose retreatment also led to impairment of autophagy, representing by downregulation of Beclin, LC3II/LC3I, and reducing the number of autophagosomes. Activation of autophagy by rapamycin could prevent high glucose-induced EMT. In addition, the levels of p62 and Snail were increased in h...
Source: Cellular Signalling - Category: Cytology Authors: Tags: Cell Signal Source Type: research