GSK3β attenuates TGF-β1 induced epithelial-mesenchymal transition and metabolic alterations in ARPE-19 cells.
作者： Li Huang , Cheng Zhang , Li Su , Zhengyu Song
DOI: 10.1016/J.BBRC.2017.03.113
关键词:
摘要: Abstract While TGF-β1 is known to induce epithelial–mesenchymal transition (EMT), a major factor in the pathogenesis of proliferative vitreoretinopathy (PVR), ARPE-19 cells. The molecular pathways involved EMT formation have not yet be fully characterized. In this study, we found that TGF-β1-mediated induction ARPE-19 cells varied dose- and time-dependent manner. Specifically, inhibited GSK-3β by accelerating phosphorylation at ser9. inhibitor or knockdown resulted enhanced EMT, migration collagen contraction ARPE-19 cells, which were then abrogated overexpression PI3K/AKT inhibitor. Importantly, also mediated metabolic reprogramming TGF-β1-treated cells. Our results indicate plays pivotal role
sci-hub.se 参考文章(28)
J. Carlos Pastor, Jimena Rojas, Salvador Pastor-Idoate, Salvatore Di Lauro, Lucia Gonzalez-Buendia, Santiago Delgado-Tirado, Proliferative vitreoretinopathy: A new concept of disease pathogenesis and practical consequences. Progress in Retinal and Eye Research. ,vol. 51, pp. 125- 155 ,(2016) , 10.1016/J.PRETEYERES.2015.07.005
Salil Kumar Bhowmik, Esmeralda Ramirez-Peña, James Michael Arnold, Vasanta Putluri, Nathalie Sphyris, George Michailidis, Nagireddy Putluri, Stefan Ambs, Arun Sreekumar, Sendurai A Mani, None, EMT-induced metabolite signature identifies poor clinical outcome. Oncotarget. ,vol. 6, pp. 42651- 42660 ,(2015) , 10.18632/ONCOTARGET.4765
Oh Woong Kwon, Ji Hun Song, Mi In Roh, Retinal Detachment and Proliferative Vitreoretinopathy. Developments in ophthalmology. ,vol. 55, pp. 154- 162 ,(2016) , 10.1159/000438972
Oksana Kaidanovich-Beilin, James Robert Woodgett, GSK-3: Functional Insights from Cell Biology and Animal Models. Frontiers in Molecular Neuroscience. ,vol. 4, pp. 40- 40 ,(2011) , 10.3389/FNMOL.2011.00040
L Jiang, L Xiao, H Sugiura, X Huang, A Ali, M Kuro-o, R J Deberardinis, D A Boothman, Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition. Oncogene. ,vol. 34, pp. 3908- 3916 ,(2015) , 10.1038/ONC.2014.321
Satoko Ishikawa, Mitsuru Nakazawa, Akira Ishikawa, Sei-Ichi Ishiguro, Makoto Tamai, Alteration of glutamine concentration in the vitreous humor in patients with proliferative vitreoretinopathy Current Eye Research. ,vol. 14, pp. 191- 197 ,(1995) , 10.3109/02713689509033514
Koji Sugioka, Aya Kodama, Kiyotaka Okada, Mihoko Iwata, Koji Yoshida, Shunji Kusaka, Chota Matsumoto, Hiroshi Kaji, Yoshikazu Shimomura, TGF-β2 promotes RPE cell invasion into a collagen gel by mediating urokinase-type plasminogen activator (uPA) expression. Experimental Eye Research. ,vol. 115, pp. 13- 21 ,(2013) , 10.1016/J.EXER.2013.06.020
F CARACI, E GILI, M CALAFIORE, M FAILLA, C LAROSA, N CRIMI, M SORTINO, F NICOLETTI, A COPANI, C VANCHERI, TGF-β1 targets the GSK-3β/β-catenin pathway via ERK activation in the transition of human lung fibroblasts into myofibroblasts Pharmacological Research. ,vol. 57, pp. 274- 282 ,(2008) , 10.1016/J.PHRS.2008.02.001
Andreas G Bader, Sohye Kang, Li Zhao, Peter K Vogt, None, Oncogenic PI3K deregulates transcription and translation. Nature Reviews Cancer. ,vol. 5, pp. 921- 929 ,(2005) , 10.1038/NRC1753
Huizhi Wang, Jonathan Brown, Michael Martin, Glycogen synthase kinase 3: a point of convergence for the host inflammatory response. Cytokine. ,vol. 53, pp. 130- 140 ,(2011) , 10.1016/J.CYTO.2010.10.009