Correction to: Cadmium exposure alters steroid receptors and proinflammatory cytokine levels in endothelial cells in vitro: a potential mechanism of endocrine disruptor atherogenic effect
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Correction to: Journal of Endocrinological Investigation https://doi.org/10.1007/s40618-018-0982-1
Unfortunately, the figure captions 4 and 6 were incorrectly published in the original publication. The complete correct captions are given below.
Figure 4 Cadmium modulation of AR-mediated signaling pathway. Representative blot which depicts AR and its phosphorylation at serine 308 (PhARser308), GSK-3β and its phosphorylation at serine 9 (PhGSK-3βser9) after 1 h of Cd exposure (a). Histograms represent the mean values of ratio of PhARser308 normalized over AR total protein level and the PhGSK-3βser9 level normalized to GSK-3β total protein content (b). Representative blot which depicts AR phosphorylation at serine 308 and AKT phosphorylation at serine 473 (PhAKTser473) in HUVECs after 1 h CdCl2 (10 μM) treatment, in the presence of GSK-3β inhibitor, AR-A014418 (10 μM) (c). Histograms represent the mean values of ratio of PhARser308 normalized over AR total protein and PhAKTser473 over total AKT (d). Effect of CdCl2 with or without DHT on HUVECs proliferation (e). Cells were incubated with or without CdCl2 (10 μM), DHT (0.01 μM) or CdCl2 in the presence of DHT for 24 and 48 h. Number of viable cells was quantified using the MTS assay. Results are presented as mean ± SD of three separate experiments. **p ≤ 0.01 and *p ≤ 0.05 vs vehicle-treated cells; §p ≤ 0.05 vs 10 μM CdCl2-treated cells.
Figure 6 Effect of ERβ blockage on proinflammatory cytokines expression. RT-qPCR showing TNFα (a), IL-6 (b), and IL-8 (c) mRNA levels of HUVECs cells exposed to CdCl2 (10 μM) or E2 (0.01 μM) in the presence or absence of PHTPP (5 μM), a selective inhibitor of ERβ.*p ≤ 0.05 and **p ≤ 0.01 vs vehicle treated cells; §§p ≤ 0.01 and §p ≤ 0.05 vs 10 μM CdCl2-treated cells.