| MicroRNA-127 Inhibits Lung Inflammation by Targeting IgG Fcγ Receptor I. | |
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MedLine Citation:
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PMID: 22287715 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. miR-127 appears to be downregulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of regulation of inflammation by miR-127, we found that IgG FcγRI (CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages overexpressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3' untranslated region of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or noninfectious lung injury. |
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Authors:
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Ting Xie; Jiurong Liang; Ningshan Liu; Qingguo Wang; Yuhang Li; Paul W Noble; Dianhua Jiang |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-1-27 |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: - ISSN: 1550-6606 ISO Abbreviation: - Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2012-1-30 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University School of Medicine, Durham, NC 27710. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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