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MicroRNA-155 is induced during the macrophage inflammatory response

O'Connell, Ryan M. and Taganov, Konstantin D. and Boldin, Mark P. and Cheng, Genhong and Baltimore, David (2007) MicroRNA-155 is induced during the macrophage inflammatory response. Proceedings of the National Academy of Sciences of the United States of America, 105 (5). pp. 1604-1609. ISSN 0027-8424. PMCID PMC1780072. doi:10.1073/pnas.0610731104.

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The mammalian inflammatory response to infection involves the induction of several hundred genes, a process that must be carefully regulated to achieve pathogen clearance and prevent the consequences of unregulated expression, such as cancer. Recently, microRNAs (miRNAs) have emerged as a class of gene expression regulators that has also been linked to cancer. However, the relationship between inflammation, innate immunity, and miRNA expression is just beginning to be explored. In the present study, we use microarray technology to identify miRNAs induced in primary murine macrophages after exposure to polyriboinosinic:polyribocytidylic acid or the cytokine IFN-{beta}. miR-155 was the only miRNA of those tested that was substantially up-regulated by both stimuli. It also was induced by several Toll-like receptor ligands through myeloid differentiation factor 88- or TRIF-dependent pathways, whereas up-regulation by IFNs was shown to involve TNF-{alpha} autocrine signaling. Pharmacological inhibition of the kinase JNK blocked induction of miR-155 in response to either polyriboinosinic:polyribocytidylic acid or TNF-{alpha}, suggesting that miR-155-inducing signals use the JNK pathway. Together, these findings characterize miR-155 as a common target of a broad range of inflammatory mediators. Importantly, because miR-155 is known to function as an oncogene, these observations identify a potential link between inflammation and cancer.

Item Type:Article
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URLURL TypeDescription CentralArticle
Boldin, Mark P.0000-0003-4593-0669
Baltimore, David0000-0001-8723-8190
Additional Information:Copyright © 2007 by the National Academy of Sciences. Freely available online through the PNAS open access option. Contributed by David Baltimore, December 4, 2006 (sent for review November 10, 2006) We thank Bruce Beutler (The Scripps Institute, La Jolla, CA) for providing TRIF mutant mice, Shizuo Akira (Osaka University, Osaka, Japan) for the MyD88-deficient mice; Arash Shahangian for help with macrophage culture and RNA preparation; and Jose Luis Riechmann, Vijaya Rao, Jaclyn Shingara, and David Brown for help with microarray work. This work was supported by the Millard and Muriel Jacobs Genetics and Genomics Laboratory at the California Institute of Technology and by grants from the National Institutes of Health. Author contributions: R.M.O. and K.D.T. designed research; R.M.O. and K.D.T. performed research; R.M.O., M.P.B., G.C., and D.B. contributed new reagents/analytic tools; R.M.O., K.D.T., M.P.B., G.C., and D.B. analyzed data; and R.M.O. and D.B. wrote the paper. The authors declare no conflict of interest. This article contains supporting information [supplementary figure 6] online at
Group:Millard and Muriel Jacobs Genetics and Genomics Laboratory
Funding AgencyGrant Number
Millard and Muriel Jacobs Genetics and Genomics LaboratoryUNSPECIFIED
Subject Keywords:cancer; inflammation; innate immunity; cytokines
Issue or Number:5
PubMed Central ID:PMC1780072
Record Number:CaltechAUTHORS:OCOpnas07
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:7249
Deposited By: Archive Administrator
Deposited On:23 Jan 2007
Last Modified:08 Nov 2021 20:40

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