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Author Huang, Li ♦ Zhang, Cheng ♦ Su, Li ♦ Song, Zhengyu
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ COLLAGEN ♦ CONTRACTION ♦ DOSES ♦ GLYCOGEN ♦ GROWTH FACTORS ♦ INDUCTION ♦ MIGRATION ♦ PATHOGENESIS ♦ PHOSPHORYLATION ♦ PHOSPHOTRANSFERASES ♦ PLANT GROWTH ♦ TIME DEPENDENCE
Abstract While TGF-β1 is known to induce epithelial–mesenchymal transition (EMT), a major factor in the pathogenesis of proliferative vitreoretinopathy (PVR), in ARPE-19 cells. The molecular pathways involved in EMT formation have not yet to be fully characterized. In this study, we have found that TGF-β1-mediated induction of EMT in ARPE-19 cells varied in a dose- and time-dependent manner. Specifically, TGF-β1 inhibited GSK-3β by accelerating phosphorylation at ser9. GSK-3β inhibitor or knockdown of GSK-3β resulted in enhanced TGF-β1-mediated EMT, migration and collagen contraction in ARPE-19 cells, which were then abrogated by GSK-3β overexpression and PI3K/AKT inhibitor. Importantly, GSK-3β also mediated metabolic reprogramming in TGF-β1-treated cells. Our results indicate that GSK-3β plays a pivotal role in TGF-β1-mediated EMT in ARPE-19 cells. - Highlights: • GSK-3β mediates epithelial-mesenchymal transition in TGF-β1 treated ARPE-19 cells. • GSK-3β regulates cell migration and collagen contraction of ARPE-19 cells. • TGF-β1 induces extracellular metabolomic changes of ARPE-19 cells via a GSK-3β-dependent mechanism.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2017-05-06
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 486
Issue Number 3


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