Editors' ChoiceAsthma

MicroRNAs, an Aquaporin Gene, and Asthma Pathogenesis

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Science Translational Medicine  20 Jun 2012:
Vol. 4, Issue 139, pp. 139ec110
DOI: 10.1126/scitranslmed.3004466

Asthma, an incurable chronic disease characterized by airway inflammation and reduced airflow, affects 22 million people in the United States, nearly one-third of whom are children. Recent studies suggest that microRNAs (miRNAs) may play a role in lung development. Jardim et al. test a related hypothesis that differences between healthy participants and those with asthma may be due to distinct miRNA profiles that result in differential regulation of inflammatory genes.

The authors examined miRNA expression in bronchial epithelial cells from seven healthy and seven asthmatic participants and identified 66 miRNAs that were significantly different between the two groups. Molecular network analysis revealed that alterations in these miRNAs from the cells of asthmatic subjects may be linked to dysregulated inflammatory pathways. During this analysis, Jardim and co-authors identified AQP4—a gene encoding a member of the aquaporin family of water-selective channels—as a previously unidentified asthma-associated gene whose expression was up-regulated in the cells from asthmatic participants. AQP4 regulates water transport across cell membranes, so it is plausible that one of the mechanisms by which the lung attempts to clear the excess fluid contributing to airway obstruction in asthma involves up-regulation of AQP4 in the bronchial epithelial cells. Although much of underlying molecular mechanisms of asthma remain to be explained, this study represents important progress in this area. It provides preliminary evidence that miRNAs may regulate transcripts of inflammatory genes involved in asthma pathogenesis, which could in turn help design better diagnostic tests and targeted therapeutics.

M. J. Jardim et al., Distinct microRNA expression in human airway cells of asthmatic donors identifies a novel asthma-associated gene. Am. J. Respir. Cell. Mol. Biol., 7 June 2012 (10.1165/rcmb.2011-0160OC). [Abstract]

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