A regulatory RNA molecule that is expressed in response to smoking is identified as a critical regulator of emphysema in a new study published online in Nature Immunology. Smoking-induced expression of the regulatory RNA miR-22 is shown to drive expression of inflammatory mediators that can lead to emphysema.
Emphysema is a chronic inflammatory lung condition that is the most predictive clinical marker of lung cancer. It is known that smoking-related emphysema is driven by T cells, but the underlying mechanisms that act on a molecular level are unknown.
David Corry, Farrah Kheradmand and colleagues find that miR-22 is expressed more in the lungs of smokers than in those of non-smokers and that mice exposed to cigarette smoke or carbon black nanoparticles, which mimic soot, also increase their expression of miR-22. The authors show that in lung immune cells, miR-22 inhibits the expression of a specific enzyme (HDAC4) in response to smoke. This enzyme prevents expression of mediators that recruit T cells and other inflammatory cells to the lung, where their activation contributes to the progressive loss of lung elasticity and function associated with emphysema. The authors show that genetically modified mice that cannot express miR-22 fail to develop disease after exposure to smoke or carbon black, revealing a link between this RNA and disease development. They conclude that selectively inhibiting miR-22 might represent a future therapy for inflammatory diseases.
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