Small Airway Epithelial Cells
The airway is lined by a layer of epithelial cells with multiple functions. In addition to providing a protective barrier function, the airway epithelium also secretes mucus and is the primary target of respiratory viruses. The airway epithelium is also the first contact point for any contaminants or pollutants that might be present in the inhaled air. For smokers, this includes irritants and inflammatory stimulants in cigarette smoke. Small airways are generally defined as those less than 2 mm in diameter and as such, are at risk for greater exposure to the damaging elements found in cigarette smoke. Dysfunction or damage to the airway epithelium can lead to chronic conditions such as asthma or chronic obstructive pulmonary disease (COPD). In particular, the study described below examines the effects of cigarette smoke on RNA expression in small airway epithelial cells.
Here at Lifeline®, we offer normal small airway epithelial cells and diseased small airway epithelial cells, which can be used to study asthma, COPD, as well as normal airway epithelial biology. Both are optimized for growth in BronchiaLife® medium, which is free of phenol red.
Lifeline® Small Airway Epithelial Cells in COPD Research
COPD is a chronic respiratory condition resulting from inflammation of the airway epithelium, which obstructs airflow. COPD results in difficulty breathing and is most often caused by smoking. In a study this year, Zeng and colleagues investigated how cigarette smoke affects the function of different RNA species to cause COPD. The researchers treated Lifeline® human small airways epithelial cells grown in BronchiaLife® medium with cigarette smoke extract or control extract, and isolated total RNA from cells to compare gene expression between both.
Overall, they isolated 4,993 circular RNAs (cirRNAs) from control cells and 903 from cells exposed to smoke extract. Of these, 65 were up-regulated and 100 were down-regulated in smoke-exposed cells compared with control. The authors also identified 3,872 and 4,425 mRNAs that were up- and down-regulated, respectively, in cells exposed to smoke extract. Further analysis demonstrated that the majority of cirRNAs were enriched at the 48 hour timepoint of smoke exposure, compared with 24 or 72 hours. Gene ontology, or GO, analysis revealed that RNAs involved in oxidative/nitrosative stress processes were enriched in cells exposed to smoke.
Additionally, the authors found that certain mRNAs they identified were also reported in tissue samples from patients with COPD, including IL6, S100A9, and SPP1. Finally, in the context of recent research suggesting that cirRNAs can act as mircoRNA (miRNA) sponges and affect gene expression, the group constructed cirRNA-mediated competitive endogenous RNA (ceRNA) networks. They found that through multiple miRNAs, around 24 cirRNAs were associated with the expression of 21 genes involved in the pentose phosphate pathway, ATP-binding cassette transporter pathways, the glycosaminoglycan biosynthesis pathway, and cancer-related pathways.
Together, the results of this study demonstrate that cirRNAs are differentially expressed in airway epithelial cells following smoke exposure. These differentially expressed cirRNAs may hold clues to the mechanism of how cigarette smoke induces COPD.
Our blog comes out every other week and highlights recent research using our products. If you have used our products in your research, we would love to hear about it. Let us know about your published study and it could be featured here on our next blog!