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Post-Transcriptional Regulation of Cystic Fibrosis Transmembrane Conductance Regulator Expression and Function by MicroRNAs
Journal article   Open access   Peer reviewed

Post-Transcriptional Regulation of Cystic Fibrosis Transmembrane Conductance Regulator Expression and Function by MicroRNAs

Shyam Ramachandran, Philip H Karp, Samantha R Osterhaus, Peng Jiang, Christine Wohlford-Lenane, Kim A Lennox, Ashley M Jacobi, Kal Praekh, Scott D Rose, Mark A Behlke, …
American journal of respiratory cell and molecular biology, Vol.49(4), pp.544-551
10/2013
DOI: 10.1165/rcmb.2012-0430OC
PMCID: PMC3824042
PMID: 23646886
url
https://doi.org/10.1165/rcmb.2012-0430OCView
Published (Version of record) Open Access

Abstract

MicroRNAs (miRNAs) are increasingly recognized as important posttranscriptional regulators of gene expression, and changes in their actions can contribute to disease states. Little is understood regarding miRNA functions in the airway epithelium under normal or diseased conditions. We profiled miRNA expression in well-differentiated primary cultures of human cystic fibrosis (CF) and non-CF airway epithelia, and discovered that miR-509–3p and miR-494 concentrations were increased in CF epithelia. Human non-CF airway epithelia, transfected with the mimics of miR-509–3p or miR-494, showed decreased cystic fibrosis transmembrane conductance regulator (CFTR) expression, whereas their respective anti-miRs exerted the opposite effect. Interestingly, the two miRNAs acted cooperatively in regulating CFTR expression. Upon infecting non-CF airway epithelial cells with Staphylococcus aureus , or upon stimulating them with the proinflammatory cytokines TNF-α or IL-1β, we observed an increased expression of both miRNAs and a concurrent decrease in CFTR expression and function, suggesting that inflammatory mediators may regulate these miRNAs. Transfecting epithelia with anti-miRs for miR-509–3p and miR-494, or inhibiting NF-κB signaling before stimulating cells with TNFα or IL-1β, suppressed these responses, suggesting that the expression of both miRNAs was responsive to NF-κB signaling. Thus, miR-509–3p and miR-494 are dynamic regulators of CFTR abundance and function in normal, non-CF airway epithelia.
cystic fibrosis transmembrane conductance regulator epithelial fluid and electrolyte transport ATP binding cassette protein 3′ UTR

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