AI Article Synopsis
- Hydroquinone (HQ) is linked to benzene-induced hematotoxicity, but the specific proteomic mechanisms are still not fully understood.
- In a study, K562 cells were treated with HQ, uncovering 187 upregulated and 279 downregulated proteins involved in various biological pathways, including immune response and cell metabolism.
- Six key proteins (STAT1, STAT3, CASP3, KIT, STAT5B, and VEGFA) were identified as significant players in erythroid differentiation-related pathways, highlighting their potential as biomarkers for HQ-induced hematotoxicity.
Article Abstract
Objective: Hydroquinone (HQ), one of the phenolic metabolites of benzene, is widely recognized as an important participant in benzene-induced hematotoxicity. However, there are few relevant proteomics in HQ-induced hematotoxicity and the mechanism hasn't been fully understood yet.
Methods: In this study, we treated K562 cells with 40 μmol/L HQ for 72 h, examined and validated protein expression changes by Label-free proteomic analysis and Parallel reaction monitoring (PRM), and performed bioinformatics analysis to identify interaction networks.
Results: One hundred and eighty-seven upregulated differentially expressed proteins (DEPs) and 279 downregulated DEPs were identified in HQ-exposed K562 cells, which were involved in neutrophil-mediated immunity, blood microparticle, and other GO terms, as well as the lysosome, metabolic, cell cycle, and cellular senescence-related pathways. Focusing on the 23 DEGs and 5 DEPs in erythroid differentiation-related pathways, we constructed the network of protein interactions and determined 6 DEPs (STAT1, STAT3, CASP3, KIT, STAT5B, and VEGFA) as main hub proteins with the most interactions, among which STATs made a central impact and may be potential biomarkers of HQ-induced hematotoxicity.
Conclusion: Our work reinforced the use of proteomics and bioinformatic approaches to advance knowledge on molecular mechanisms of HQ-induced hematotoxicity at the protein level and provide a valuable basis for further clarification.
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| http://dx.doi.org/10.3967/bes2024.039 | DOI Listing |
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