Abstract
Background: Pulmonary morbidity and mortality resulting from exposure to diesel exhaust particle (DEP) increases with age. In addition, we previously reported that oxidative stress by cigarette smoke induced aging phenotype of epithelial cells via miRNA34a dependent reduction of SIRT1, a NAD+ -dependent Class 3 histone deacetylase, which is known to be down-regulated in COPD patients.
Aims: To investigate the effects of DEP on aging phenotype of primary epithelial cells and anti-aging molecule, sirtuin, expression.
Methods: Primary bronchial epithelial cells were incubated with DEP for 48hrs and β-galactosidase was detected by cytochemistry. After DEP treatment to BEAS2B human airway epithelial cells for 48 and 78 hrs, protein expression of SIRT1 and SIRT6 were determined by western blotting, and miRNA34a was detected by PCR.
Results: DEP (2.5 – 40 µg/ml) increased β-galactosidase positive aged primary bronchial cells in a concentration dependent manner. DEP (5µg/ml) also increased miRNA34a after 72hrs incubation, leading reduction of mRNA and protein expression of SIRT1 and SIRT6.
Conclusions: DEP exposure increased bronchial cell senescence via SIRT1/SIRT6 reduction by elevation of miRNA34a. Thus DEP exposure is a potential risk of accelerating aging of lung.
Footnotes
Cite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA2348.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2019