Fig. 7: Inhibition of galectin-3 expression ameliorates the EndMT process by downregulating the AKT/β-catenin pathway in HPMECs. | Cell Death & Disease

Fig. 7: Inhibition of galectin-3 expression ameliorates the EndMT process by downregulating the AKT/β-catenin pathway in HPMECs.

From: Trajectory modeling of endothelial-to-mesenchymal transition reveals galectin-3 as a mediator in pulmonary fibrosis

Fig. 7

A Schematic showing the knockdown of galectin-3 expression with siRNA, and its impact on the transition of HPMECs. HPMECs were first cultured in complete medium for 24 h, and then transfected with siRNA targeting galectin-3 for 6 h. After treatment with the siRNA, the complete medium was replaced with starvation medium (DMEM containing 1% FBS), followed by further cultivation for 48 h. B The knockdown efficiency of galectin-3 siRNA according to RT-PCR. siNC: negative control. C–G HPMECs were stimulated with TGF-β (10 ng/ml, S + T) or galectin-3 (1 μg/ml, S + G) and interfered with galectin-3 siRNA (S + T + galectin-3 siRNA and S + G + galectin-3 siRNA, respectively) for 48 h. Analysis of the expression level analysis of the target genes galectin-3, β-catenin, and SMAD2, as well as the fibroblast-related genes α-SMA and S100A in different experimental groups using RT-PCR. Error bars represent standard deviations, n = 3. H HPMECs lysate was analyzed for CD31, α-SMA, and AKT/β-catenin signaling pathway regulators, total AKT and pS473 AKT, total-β-catenin and pY654 β-catenin, PI3K and GSK3β by Western blotting. *p < 0.05, **p < 0.01, ***p < 0.001.

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