Nrf2-Heme Oxygenase-1 Attenuates High-Glucose-Induced Epithelial-to-Mesenchymal Transition of Renal Tubule Cells by Inhibiting ROS-Mediated PI3K/Akt/GSK-3<i>β</i> Signaling

<div>HG-induced EMT: a change of morphologic phenotype in human HK2 cells. Representative photomicrograph shows round- to oval-shaped growth in normal renal tubular cells, which converted into bipolar- or spindle-shaped cells with a fibroblast-like morphology after continuous stimulation with high glucose (60 mM/L D-glucose) for 72 h (right ×200, left ×100). (a) Exposure of HK2 cells to HG decreased the protein expression of the epithelial cell marker E-cadherin and increased the expression of the mesenchymal markers vimentin and fibronectin. (b) Cell viability exclusion assay by trypan blue staining. The number of trypan blue-positive cells was increased at a concentration-dependent manner in HG-treated HK2 cells (c).</div>

Journal of Diabetes Research

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Figure 1

Figure 1: Nrf2-Heme Oxygenase-1 Attenuates High-Glucose-Induced Epithelial-to-Mesenchymal Transition of Renal Tubule Cells by Inhibiting ROS-Mediated PI3K/Akt/GSK-3<i>β</i> Signaling 

Figure 1 | Nrf2-Heme Oxygenase-1 Attenuates High-Glucose-Induced Epithelial-to-Mesenchymal Transition of Renal Tubule Cells by Inhibiting ROS-Mediated PI3K/Akt/GSK-3β Signaling 