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. 2018 May 20;19(5):1525. doi: 10.3390/ijms19051525

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Phosphorylated ERK1/2 protein levels in human pulmonary artery endothelial cells (HPAECs) exposed to hyperoxia. HPAECs were exposed to normoxia or hyperoxia for 24 or 48 h, following which whole-cell proteins were extracted, and immunoblotting was performed using antibodies against total ERK1/2, phosphorylated ERK1/2, or β-actin. Representative immunoblot showing total ERK1/2 and phosphorylated ERK1/2 protein expression (A). Densitometric analyses wherein the phosphorylated ERK1/2 band intensities were quantified and normalized to those of total ERK1/2 (B). The values are presented as mean ± SD (n = 6/group). Two-way ANOVA analysis showed an effect of hyperoxia and duration of exposure and an interaction between them for the dependent variable, p-ERK1/2, in this figure. Significant differences between normoxia- and hyperoxia-exposed cells are indicated by * p < 0.001. Significant differences between hyperoxia-exposed cells are indicated by † p < 0.01 (Two-way ANOVA).