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JCR 2016
جستجوی مقالات
چهارشنبه 19 آذر 1404
Iranian Journal of Basic Medical Sciences
، جلد ۲۵، شماره ۴، صفحات ۴۷۴-۴۸۲
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عنوان انگلیسی
Induced overexpression of MARCH-1 in human macrophages altered to M2 phenotype for suppressing inflammation process
چکیده انگلیسی مقاله
Objective(s): The M1 macrophage is characterized by enhanced pro-inflammatory cytokines production, whereas macrophage (M2) has anti-inflammatory features. Macrophage polarization as a therapeutic target for controlling immune responses could be performed by gene transduction to control the regulation of exaggerated innate/adaptive immune responses. Materials and Methods: Macrophages were prepared from THP-1 cell line and human monocytes that were transduced with (Membrane-Associated RING-CH-type finger) MARCH-1 viral lentivector produced in HEK-293T cells. RT-PCR and Western blotting confirmed MARCH-1 gene transduction. Cytokine production, CD markers assay, macrophage phagocytosis potential activity and mixed leukocyte reaction (MLR) with CFSE were performed for M1/M2 plasticity.Results: The mean fluorescent intensity of HLA-DR and CD64 expression reduced in MARCH-1+ transduced macrophage population. However, CD206 and CD163 expression increased in these macrophages. The concentrations of IL-6, TNF-α and iNOS were decreased in MARCH-1 transduced cells, and TGF-β production showed an augmentation in concentration. Western blotting and real-time PCR measurement confirmed that the expression levels of MARCH-1 protein and arginase-1 enzyme were increased in transduced macrophages.Conclusion: The anti-inflammatory features of MARCH-1 revealed the reduced levels of pro-inflammatory factors and maintained M2 phenotype characterized by high levels of scavenger receptors. Therefore, targeting MARCH-1 in monocytes/macrophages could represent a new autologous cell-based therapies strategy for inflammatory conditions.
کلیدواژههای انگلیسی مقاله
INOS, Macrophage, MARCH-1, Polarization, TGF-beta
نویسندگان مقاله
| Zivar Zangeneh
Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
| Gholamreza Khamisipour
Department of Hematology, School of Para Medicine, Bushehr University of Medical Sciences, Bushehr, Iran
| Alireza Andalib
Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran|National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran
نشانی اینترنتی
https://ijbms.mums.ac.ir/article_20078.html
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Original Article
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