Fig. 1: Increased epithelial-to-mesenchymal transition (EMT) via activation of the Smad2/3 signaling pathways and NOX2/4-induced ROS generation in HPMCs treated with TGF-β1. | Cell Death & Disease

Fig. 1: Increased epithelial-to-mesenchymal transition (EMT) via activation of the Smad2/3 signaling pathways and NOX2/4-induced ROS generation in HPMCs treated with TGF-β1.

From: Autophagy caused by oxidative stress promotes TGF-β1-induced epithelial-to-mesenchymal transition in human peritoneal mesothelial cells

Fig. 1

A TGF-β1 treatment (2 [T2] and 5 [T5] ng/mL) increased mRNA expression of the profibrotic mesenchymal markers (E-cadherin, fibronectin, and α-SMA) in HPMCs. B, C TGF-β1 treatment (2 and 5 ng/mL) increased protein levels of the profibrotic mesenchymal markers and activated the phosphorylation of Smad2/3 signaling in HPMCs. D TGF-β1 treatment (2 and 5 ng/mL) increased the mRNA expression of NOX2/4 and P22phox in HPMCs after 48 h. E TGF-β1 induced ROS generation, which was measured using DCF-DA 1 h after TGF-β1 treatment (2 and 5 ng/mL). F TGF-β1 induced H2O2 generation 24 h after treatment (2 and 5 ng/mL). The data are presented as mean ± standard error. n = 4 per group. *P < 0.05 vs. control (C); **P < 0.01 vs. control; and ***P < 0.001 vs. control.

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