Altered long non-coding RNAs expression in normal and diseased primary human airway epithelial cells exposed to diesel exhaust particles

Abstract

Background

Exposure to diesel exhaust particles (DEP) has been linked to a variety of adverse health effects, including increased morbidity and mortality from cardiovascular diseases, chronic obstructive pulmonary disease (COPD), metabolic syndrome, and lung cancer. The epigenetic changes caused by air pollution have been associated with increased health risks. However, the exact molecular mechanisms underlying the lncRNA-mediated pathogenesis induced by DEP exposure have not been revealed.

Methods

Through RNA-sequencing and integrative analysis of both mRNA and lncRNA profiles, this study investigated the role of lncRNAs in altered gene expression in healthy and diseased human primary epithelial cells (NHBE and DHBE-COPD) exposed to DEP at a dose of 30 μg/cm².

Results

We identified 503 and 563 differentially expressed (DE) mRNAs and a total of 10 and 14 DE lncRNAs in NHBE and DHBE-COPD cells exposed to DEP, respectively. In both NHBE and DHBE-COPD cells, enriched cancer-related pathways were identified at mRNA level, and 3 common lncRNAs OLMALINC, AC069234.2, and LINC00665 were found to be associated with cancer initiation and progression. In addition, we identified two cis-acting (TMEM51-AS1 and TTN-AS1) and several trans-acting lncRNAs (e.g. LINC01278, SNHG29, AC006064.4, TMEM51-AS1) only differentially expressed in COPD cells, which could potentially play a role in carcinogenesis and determine their susceptibility to DEP exposure.

Conclusions

Overall, our work highlights the potential importance of lncRNAs in regulating DEP-induced gene expression changes associated with carcinogenesis, and individuals suffering from COPD are likely to be more vulnerable to these environmental triggers.

Keywords:

• Diesel exhaust particle
• COPD
• lncRNAs
• lncRNA-mRNA interaction
• carcinogenesis
• susceptibility

View correction statement:

Correction

Acknowledgements

Ying-Hsuan Lin gratefully acknowledges the support from the University of California, Riverside (UCR) Regents’ Faculty Fellowships for this research.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Code availability

Data analysis and codes are available at https://github.com/biplabua/DEP_lncRNA_mRNA_Co-expression_2021.

Data availability statement

The authors confirm that the data supporting the findings of this study are available within the article and its supplementary materials.

Correction Statement

This article was originally published with errors, which have now been corrected in the online version. Please see Correction (http://dx.doi.org/10.1080/08958378.2023.2245658).

Additional information

Funding

Alexa Canchola was supported by an NRSA T32 training grant [T32 ES018827].