2014 Volume 39 Issue 3 Pages 487-497
Crotonaldehyde, a highly toxic α, β-unsaturated aldehyde, is a major component of cigarette smoke and a ubiquitous environmental pollutant. Crotonaldehyde exposure is known to have adverse effects on respiratory health, but the underlying mechanisms remain obscure. As alveolar macrophages display important immunological and inflammatory properties in response to extraneous substances in the lung, we aimed at gaining more insight in changes of human macrophage-like cells transcriptome in response to crotonaldehyde. In vitro cultures of human THP-1 cells (a human monocytic leukemia cell line) were differentiated into macrophage-like cells treated by PMA (phorbol 12-myristate 13-acetate) and be exposed crotonaldehyde. Using RNA-seq technology such as digital gene expression, the global changes in transcriptional level were analyzed. Real-time quantitative polymerase chain reaction (qPCR) was performed to validate RNA-seq data. The differential regulated genes in many biological processes were dysregulated, including in antigen processing and presentation, oxidative stress, inﬂammation, cytokine signaling, and apoptosis. Collectively, our study demonstrated that crotonaldehyde altered gene expression proﬁle in the genome-wide transcriptional level in human macrophage-like cells, and many of them may represent potential mechanisms of crotonaldehyde causing cytotoxicity and tissue injury in the human lung.