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      A Review of Macrophage MicroRNAs’ Role in Human Asthma

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          Abstract

          There is an imbalance in asthma between classically activated macrophages (M1 cells) and alternatively activated macrophages (M2 cells) in favor of the latter. MicroRNAs (miRNAs) play a critical role in regulating macrophage proliferation and differentiation and control the balance of M1 and M2 macrophage polarization, thereby controlling immune responses. Here we review the current published data concerning miRNAs with known correlation to a specific human macrophage phenotype and polarization, and their association with adult asthma. MiRNA-targeted therapy is still in the initial stages, but clinical trials are under recruitment or currently running for some miRNAs in other diseases. Regulating miRNA expression via their upregulation or downregulation could show potential as a novel therapy for improving treatment efficacy in asthma.

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

          Jonathan B Johnnidis, Marian Harris, Robert Wheeler … (2008)
          MicroRNAs are abundant in animal genomes and have been predicted to have important roles in a broad range of gene expression programmes. Despite this prominence, there is a dearth of functional knowledge regarding individual mammalian microRNAs. Using a loss-of-function allele in mice, we report here that the myeloid-specific microRNA-223 (miR-223) negatively regulates progenitor proliferation and granulocyte differentiation and activation. miR-223 (also called Mirn223) mutant mice have an expanded granulocytic compartment resulting from a cell-autonomous increase in the number of granulocyte progenitors. We show that Mef2c, a transcription factor that promotes myeloid progenitor proliferation, is a target of miR-223, and that genetic ablation of Mef2c suppresses progenitor expansion and corrects the neutrophilic phenotype in miR-223 null mice. In addition, granulocytes lacking miR-223 are hypermature, hypersensitive to activating stimuli and display increased fungicidal activity. As a consequence of this neutrophil hyperactivity, miR-223 mutant mice spontaneously develop inflammatory lung pathology and exhibit exaggerated tissue destruction after endotoxin challenge. Our data support a model in which miR-223 acts as a fine-tuner of granulocyte production and the inflammatory response.
          Article 0 comments Cited 373 times – based on 0 reviews     Review now
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            Negative regulation of TLR4 via targeting of the proinflammatory tumor suppressor PDCD4 by the microRNA miR-21.

            Frederick J. Sheedy, Eva M. Pålsson-McDermott, Elizabeth J Hennessy … (2010)
            The tumor suppressor PDCD4 is a proinflammatory protein that promotes activation of the transcription factor NF-kappaB and suppresses interleukin 10 (IL-10). Here we found that mice deficient in PDCD4 were protected from lipopolysaccharide (LPS)-induced death. The induction of NF-kappaB and IL-6 by LPS required PDCD4, whereas LPS enhanced IL-10 induction in cells lacking PDCD4. Treatment of human peripheral blood mononuclear cells with LPS resulted in lower PDCD4 expression, which was due to induction of the microRNA miR-21 via the adaptor MyD88 and NF-kappaB. Transfection of cells with a miR-21 precursor blocked NF-kappaB activity and promoted IL-10 production in response to LPS, whereas transfection with antisense oligonucleotides to miR-21 or targeted protection of the miR-21 site in Pdcd4 mRNA had the opposite effect. Thus, miR-21 regulates PDCD4 expression after LPS stimulation.
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              MiRNA-Mediated Macrophage Polarization and its Potential Role in the Regulation of Inflammatory Response.

              Kobina Essandoh, Yutian Li, Jiuzhou Huo … (2016)
              Monocytes and macrophages are important components of the immune system, specialized in either removing pathogens as part of innate immunity or contributing to adaptive immunity through antigen presentation. Essential to such functions is classical activation (M1) and alternative activation (M2) of macrophages. M1 polarization of macrophages is characterized by production of pro-inflammatory cytokines, antimicrobial and tumoricidal activity, whereas M2 polarization of macrophages is linked to immunosuppression, tumorigenesis, wound repair, and elimination of parasites. MiRNAs are small non-coding RNAs with the ability to regulate gene expression and network of cellular processes. A number of studies have determined miRNA expression profiles in M1 and M2 polarized human and murine macrophages using microarray and RT-qPCR arrays techniques. More specifically, miR-9, miR-127, miR-155, and miR-125b have been shown to promote M1 polarization while miR-124, miR-223, miR-34a, let-7c, miR-132, miR-146a, and miR-125a-5p induce M2 polarization in macrophages by targeting various transcription factors and adaptor proteins. Further, M1 and M2 phenotypes play distinctive roles in cell growth and progression of inflammation-related diseases such as sepsis, obesity, cancer, and multiple sclerosis. Hence, miRNAs that modulate macrophage polarization may have therapeutic potential in the treatment of inflammation-related diseases. This review highlights recent findings in miRNA expression profiles in polarized macrophages from murine and human sources, and summarizes how these miRNAs regulate macrophage polarization. Last, therapeutic potential of miRNAs in inflammation-related diseases through modulation of macrophage polarization is also discussed.
              Article 0 comments Cited 265 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 08 May 2019
                Publication date Collection: May 2019
                Volume: 8
                Issue: 5
                Electronic Location Identifier: 420
                Affiliations
                [1 ]Department of Hematology, Iuliu Haţieganu University of Medicine and Pharmacy, 400124 Cluj-Napoca, Romania; Fechetea.Gabriela@ 123456umfcluj.ro (G.F.); popescu.cristian@ 123456umfcluj.ro (C.P.)
                [2 ]Department of Pharmacology, Toxicology and Clinical Pharmacology, Iuliu Haţieganu University of Medicine and Pharmacy, 400337 Cluj-Napoca, Romania; bocsan.corina@ 123456umfcluj.ro
                [3 ]Department of Hematology, Carol Davila University of Medicine and Pharmacy, 050474 Bucharest, Romania; mihaela_dervesteanu@ 123456yahoo.com
                [4 ]National Heart and Lung Institute, Imperial College London, London W2 1PG, UK
                [5 ]Department of Hematology, Ion Chiricuta Oncology Institute, 400010 Cluj-Napoca, Romania
                Author notes
                [†]

                These authors contributed equally to this paper.

                Author information
                https://orcid.org/0000-0001-9026-2597
                https://orcid.org/0000-0003-3015-9023
                https://orcid.org/0000-0002-9461-987X
                Article
                Publisher ID: cells-08-00420
                DOI: 10.3390/cells8050420
                PMC ID: 6562863
                PubMed ID: 31071965
                SO-VID: 4bae3113-6a15-4b30-b959-7ab8c4127ca1
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 01 April 2019
                Date accepted : 07 May 2019
                Categories
                Subject: Review

                Keywords: asthma,molecular asthma,macrophages,microrna
                Data availability:
                Keywords: asthma, molecular asthma, macrophages, microrna

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