Abstract

Pulmonary fibroblasts are important structural lung cells that modulate tissue injury and immune response. It plays an important role in the inflammatory response by interacting between pulmonary fibroblasts and leukocytes. Cigarette smoke is known to trigger the development of diverse pulmonary and lung diseases, such as chronic obstructive pulmonary disease (COPD). α,β-unsaturated aldehydes such as acrolein (ACR) are present in cigarette smoke and are environment pollutants. ACR induces dysfunction of pulmonary and lung cells by forming DNA adducts and releasing inflammatory cytokines. MicroRNAs (miRNAs) are small interfering RNAs that negatively regulate mRNA gene expression and control the cellular response to toxic compounds. mRNAs also post-transcriptionally modulate gene expression. In this study, we identified whether the effects of ACR on the expression pattern of miRNAs in human pulmonary fibroblasts (HPFs). We carried out a pair-wise correlation analysis and examined 22 and 31 miRNAs with changed expression levels after treatment of HPFs with 10 μM and 25 μM ACR, respectively. Furthermore, we identified a significant anti-correlation in 102 and 17 mRNAs. Differentially expressed miRNAs and signaling pathways were further analyzed by gene ontology enrichment analysis. Our results showed that altered expression of miRNAs by ACR treatment was relevant in the dysfunction of respiratory cells and might contribute to the understanding of the mechanism of pulmonary diseases.

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