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1. NFκB-Mediated Expression of Phosphoinositide 3-Kinase δ Is Critical for Mesenchymal Transition in Retinal Pigment Epithelial Cells

Author

Haote Han, Yanhui Yang, Zhuo Han, Luping Wang, Lijun Dong, Hui Qi, Bing Liu, Jingkui Tian, Bart Vanhaesebroeck, Andrius Kazlauskas, Guoming Zhang, Shaochong Zhang, and Hetian Lei

Subjects
TGF-β2, PI3Kδ, NFκB/p65, CRISPR/Cas9, RPE, EMT, Cytology, QH573-671
Abstract

Epithelial mesenchymal transition (EMT) plays a vital role in a variety of human diseases including proliferative vitreoretinopathy (PVR), in which retinal pigment epithelial (RPE) cells play a key part. Transcriptomic analysis showed that the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway was up-regulated in human RPE cells upon treatment with transforming growth factor (TGF)-β2, a multifunctional cytokine associated with clinical PVR. Stimulation of human RPE cells with TGF-β2 induced expression of p110δ (the catalytic subunit of PI3Kδ) and activation of NFκB/p65. CRISPR-Cas9-mediated depletion of p110δ or NFκB/p65 suppressed TGF-β2-induced fibronectin expression and activation of Akt as well as migration of these cells. Intriguingly, abrogating expression of NFκB/p65 also blocked TGF-β2-induced expression of p110δ, and luciferase reporter assay indicated that TGF-β2 induced NFκB/p65 binding to the promoter of the PIK3CD that encodes p110δ. These data reveal that NFκB/p65-mediated expression of PI3Kδ is essential in human RPE cells for TGF-β2-induced EMT, uncovering hindrance of TGF-β2-induced expression of p110δ as a novel approach to inhibit PVR.

Published
2023
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2. Chalcomoracin Prevents Vitreous-Induced Activation of AKT and Migration of Retinal Pigment Epithelial Cells

Author

Jiantao Wang, Wei Zhu, Haote Han, Yanhui Yang, Bing Liu, Jingkui Tian, and Hetian Lei

Subjects
Proliferative vitreoretinopathy, Contraction (grammar), Chemistry, Retinal, medicine.disease, eye diseases, 3. Good health, Cell biology, Pigment, chemistry.chemical_compound, visual_art, visual_art.visual_art_medium, medicine, biochemistry, Chalcomoracin, sense organs, Protein kinase B
Abstract

Retinal pigment epithelial (RPE) cells are the major cell type in the epi- or sub-retinal membranes in the pathogenesis of proliferative vitreoretinopathy (PVR), which is a blinding fibrotic eye disease and still short of effective medicine. The purpose of this study is to demonstrate if Chalocomoracin (CMR), a novel purified compound from fungus-infected mulberry leaves, is able to inhibit vitreous-induced signaling events and cellular responses intrinsic to PVR. Our studies have revealed that the CMR IC50 for ARPE-19 cells is 35.5 μM at 72 hours, and that 5 μM CMR inhibits vitreous-induced Akt activation and p53 suppression; in addition we have discovered that this chemical effectively blocks vitreous-stimulated proliferation, migration and contraction of ARPE-19 cells, suggesting that CMR is a promising PVR prophylactic.

Published
2020
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