Regulation of progenitor cell proliferation and granulocyte function by microRNA-223

By Jonathan B. Johnnidis, M. Harris, R. Wheeler, Sandra Stehling-Sun, Michael H Lam, O. Kirak, T. Brummelkamp, M. Fleming, F. Camargo. Nature, 2008

1,238 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/2abee619d9ecc3c1112807f6f500da66307440c0

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Citations in the corpus

NLRP3 inflammasome and its inhibitors: a review (2015, background): “Deficiency in microRNA-223 leads to neutrophilia, spontaneous lung inflammation, and increased susceptibility to endotoxin Frontiers in Pharmacology | www.frontiersin.org 5 November 2015 | Volume 6 | Article 262 challenge in mice (Johnnidis et al., 2008; Haneklaus et al., 2013).”
Detection of microRNA Expression in Human Peripheral Blood Microvesicles (2008, background): “miR-223 also appears to have a role in hematopoietic stem cell proliferation [43].”
MicroRNA profiling of multiple sclerosis lesions identifies modulators of the regulatory protein CD47. (2009, background): “Myocyte enhancer factor-2c, a transcription factor that promotes (among other features) myeloid progenitor proliferation, is a proven target of miR-223 (Johnnidis et al., 2008).”
MicroRNAs: new regulators of immune cell development and function (2008, background): “Its expression changes during maturation, becoming incrementally higher as granulocytes matur”
MicroRNAs in development and disease. (2011, background): “Whereas let-7 is known for its tumor suppressive function via targeting c-myc in lymphoma cells (526), miR-223 has been shown to increase during granulocyte differentiation (281) and is sufficient for inducing differentiation of myeloid leukemia cells when ectopically expressed (172).”
Biological functions of microRNAs: a review (2011, background): “Thus, miR-223 acts as a fine-tuner of granulocyte production and the inflammatory response [ 19 ].”
Inositol phosphatase SHIP1 is a primary target of miR-155 (2009, background): “Similar observations have been made for specific targets of miR-150 (11, 50), miR-223 (6), and miR-17–92 (10, 12), suggesting a common theme of a few significant targets making dominant contributions to miRNA function.”
microRNA regulation of inflammatory responses. (2012, background): “For instance, mice deficient in miR-223 have increased responses to fungal pathogens owing to hyperactivation of granulocytes (68).”
The Role of MicroRNAs in Human Diseases (2010, background): “Finally, the myeloid-specific miR-223 is reported to be involved in regulation of granulocyte differentiation and activation during inflammation (62, 97) .”
Microvesicles secreted by macrophages shuttle invasion-potentiating microRNAs into breast cancer cells (2011, background): “Previous studies have suggested that miR-223 targets the myocyte enhancer factor, Mef2c, in myeloid progenitor cells to inhibit their proliferation and granulocyte function [28].”
An overview of microRNAs (2015, background): “miRNAs have been linked to the function of many hematopoietic lineages including neutrophils, lymphocytes, erythrocytes, megakaryocytes, an hematopoetic stem cells [17, 150-161].”
MicroRNA-124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP-α–PU.1 pathway (2010, neutral): “miRNAs have been identified as crucial regulators of differentiation of various cell types, including neuronal cells in the central nervous system (CNS) and myeloid cells in the innate immune syste”
Metazoan MicroRNAs (2018, background): “…neutrophils and macrophages; increased spontaneous and induced lung pathology (after endotoxin challenge); altered susceptibility to infection (Johnnidis et al., 2008; Zhuang et al., 2012; Lu et al., 2013a); increased serum cholesterol and triglycerides (Vickers et al., 2014); altered…”
Physiological and pathological roles for microRNAs in the immune system (2010, background): “, and it negatively regulates both the proliferation and activation of neutrophil”
microRNAs and the immune response (2009, background): “This conclusion is based upon observations in a miR-223 knockout mouse, which demonstrated increased neutrophil numbers, spontaneous inflammation in the lung and exaggerated tissue destruction following LPS challenge [17].”