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Fig. 1 | Clinical Proteomics

Fig. 1

From: Proteomics-based evaluation of the mechanism underlying vascular injury via DNA interstrand crosslinks, glutathione perturbation, mitogen-activated protein kinase, and Wnt and ErbB signaling pathways induced by crotonaldehyde

Fig. 1

The effects of crotonaldehyde (CRA) on human aortic endothelial cells (HAECs). A DNA damage induced by CRA in HAECs deficient in the FANC pathway. HAECs were exposed to a range of CRA concentrations—0, 0.5, 1, 2, 3, and 4 μM—and incubated for a period of 8 days. Drug lethal dose (LD50) values were identified from data generated using survival curves and have been indicated by an arrow. Data are expressed as mean ± standard deviation of five independent experiments. B Effect of CRA on the depletion of mitochondrial membrane potential. C Effect of CRA on GSH levels. D Activation of COX-2 by CRA. E Activation of MAPK pathways, including P-ERK, P-JNK, and P-P38, by CRA. Data are expressed as mean ± standard deviation of three independent experiments (B–E); statistically significant differences are indicated by an asterisk; p < 0.05 was considered statistically significant

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Clinical Proteomics

ISSN: 1559-0275