作者: Jinyan Li , Yijia Chen , Chenlu Han , Shan Huang , Shuyi Chen
DOI: 10.1016/J.BBRC.2019.02.049
关键词:
摘要: Abstract Epithelial-mesenchymal transition (EMT) is the main cause of fibrotic cataracts. Oxidative stress was recently shown to trigger epithelial-mesenchymal in human lens epithelial cells (hLECs). However, underlying mechanism not fully understood. Here we reported that exposure low doses (100 μM) H2O2 led EMT hLECs, as indicated by simultaneous down-regulated E-cadherin and ZO-1, up-regulated alpha smooth muscle actin (α-SMA). H2O2-induced accompanied accumulation phosphorylated JNK1. In contrast, knockdown JNK1 via siRNA reversed EMT. Of interest, capsules anterior subcapsule cataracts, expressions JNK1, well β-catenin its downstream effectors cyclin D c-Myc, were augmented compared normal capsules. Mechanistically, activated dislodged from cell membrane, which subsequently translocated nuclei triggered transcription effectors. Nuclei β-catenin, c-Myc accumulated depletion abrogated these trend hLECs. conclusion, our data suggest essential for hLECs mediating translocation β-catenin.