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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

Crotonaldehyde (CRA)—one of the major environmental pollutants from tobacco smoke and industrial pollution—is associated with vascular injury (VI). We used proteomics to systematically characterize the presently unclear molecular mechanism of VI and to identify new related targets or signaling pathw...

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Published in:Clinical proteomics 2022-08, Vol.19 (1), p.1-33, Article 33
Main Authors: Xie, Ming-Zhang, Liu, Jun-Li, Gao, Qing-Zu, Bo, De-Ying, Wang, Lei, Zhou, Xiao-Chun, Zhao, Meng-Meng, Zhang, Yu-Chao, Zhang, Yu-Jing, Zhao, Guo-An, Jiao, Lu-Yang
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Language:English
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Summary:Crotonaldehyde (CRA)—one of the major environmental pollutants from tobacco smoke and industrial pollution—is associated with vascular injury (VI). We used proteomics to systematically characterize the presently unclear molecular mechanism of VI and to identify new related targets or signaling pathways after exposure to CRA. Cell survival assays were used to assess DNA damage, whereas oxidative stress was determined using colorimetric assays and by quantitative fluorescence study; additionally, cyclooxygenase-2, mitogen-activated protein kinase pathways, Wnt3a, β-catenin, phospho-ErbB2, and phospho-ErbB4 were assessed using ELISA. Proteins were quantitated via tandem mass tag-based liquid chromatography-mass spectrometry and bioinformatics analyses, and 34 differentially expressed proteins were confirmed using parallel reaction monitoring, which were defined as new indicators related to the mechanism underlying DNA damage; glutathione perturbation; mitogen-activated protein kinase; and the Wnt and ErbB signaling pathways in VI based on Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and protein–protein interaction network analyses. Parallel reaction monitoring confirmed significant (p  1.5-fold change) of 23 proteins and downregulation (
ISSN:1542-6416
1559-0275
DOI:10.1186/s12014-022-09369-7