MicroRNA-221 is overexpressed in the equine asthmatic airway smooth muscle and modulates smooth muscle cell proliferation.

This research article investigates the role of microRNA-221 in the airway smooth muscle of asthmatic horses, finding that this particular microRNA becomes overexpressed during asthma flare-ups. The study’s findings suggest that microRNA-221 contributes to cell proliferation in the airway smooth muscle, which could offer up new avenues for treating airway remodeling in asthma.

Background

• Asthma is a chronic inflammatory disease of the airways, leading to airflow obstruction due to swelling and increased mucus production in the airway. One major characteristic of asthma is the thickening of the airways (also known as airway remodeling) caused by proliferation of airway smooth muscle (ASM) cells.
• MicroRNAs (miRNAs) are a type of regulatory RNA molecule that can block the translation of messenger RNAs (mRNAs) into proteins. The researchers suggest that miRNAs could be involved in the remodeling process in asthma by influencing ASM cell proliferation.

Methods

• The researchers collected bronchial smooth muscle samples from both horses with exacerbated asthma and horses in asthma remission. They compared the miRNA expression in these samples with that in healthy controls.
• They then conducted further experiments to study the effect of specific miRNAs on ASM cell proliferation.

Results

• The results showed that miRNAs miR-26a, miR-133, and miR-221 were overexpressed in the ASM cells of horses with exacerbated asthma. In particular, miR-221 induced hyperproliferation of ASM cells and reduced the expression of genes that usually limit cell proliferation.
• The researchers drew attention to miR-221, as their findings indicated that it contributes to the overgrowth of ASM cells during asthma flare-ups by inhibiting the expression of cell cycle regulatory genes.

Conclusion

• This study suggests that miR-221 could be a key player in the airway remodeling observed in asthma. It offers preliminary evidence that targeting the network of genes regulated by miR-221 could be a novel approach for treating ASM remodeling in asthma.