miR-142-5p and miR-130a-3p are regulated by IL-4 and IL-13 and control profibrogenic macrophage program

Su, Shicheng; Zhao, Qiyi; He, Chonghua; Huang, Di; Liu, Jiang; Chen, Fei; Chen, Jianing; Liao, Jiayuan; Cui, Xiaona; Zeng, Yonghong; Yao, Herui; Su, Fengxi; Liu, Qiang; Jiang, Shanping; Song, Erwei

doi:10.1038/ncomms9523

Cited by 220 publications

(207 citation statements)

References 60 publications

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“…One possibility is that microRNAs (miRs) play a role in regulating expression of these transcripts. Support for this possibility was recently reported in a study were human monocyte-derived macrophages treated with IL-4/IL-13 displayed increased miR-142-5p and decreased miR-130-3p [13]. In the activation model used in this study, miR-142-5p regulated the phosphorylation of STAT6.…”

Section: Introductionsupporting

confidence: 77%

Nanoparticle delivery of miR-223 to attenuate macrophage fusion

et al. 2016

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The foreign body response (FBR) begins with injury acquired during implantation of a biomaterial (BM) and is detrimental due to the eventual encapsulation of the implant. Fusion of macrophages to form foreign body giant cells (FBGC), a hallmark of the FBR, is the consequence of a multistep mechanism induced by interleukin (IL)-4 that includes the acquisition of a fusion competent state and subsequent cytoskeletal rearrangements. However, the precise mechanism, regulation, and interplay among molecular mediators to generate FBGCs are insufficiently understood. Seeking novel mediators of fusion that might be regulated at the post-transcriptional level, we examined the role of microRNAs (miRs) in this process. A miR microarray was screened and identified miR-223 as a negative regulator of macrophage fusion. In addition, transfection of primary macrophages with a mir-223 mimic attenuated IL-4-induced fusion. Furthermore, miR-223 KO mice and mir-223 deficient cells displayed increased fusion in vivo and in vitro, respectively. Finally, we developed a method for in vivo delivery of miR-223 mimic utilizing PLGA nanoparticles, which inhibited FBGC formation in a biomaterial implant model. Our results identify miR-223 as a negative regulator of fusion and demonstrate miR-223 mimic-loaded nanoparticles as a therapeutic inhibitor of macrophage fusion.

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Section: Introductionsupporting

confidence: 77%

Nanoparticle delivery of miR-223 to attenuate macrophage fusion

et al. 2016

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“…Notably, if we focus on in vivo human studies, the majority of dysregulated miRs were identified by evaluating whole-lung explants (55)(56)(57)(58)(59)(60)(61)(62)(63)(64). However, the whole lung has multiple cell types (e.g., epithelium, fibroblast, macrophage) that participated in fibroproliferation, and only a limited number of studies confirm the in vivo cellular compartment with dysregulated miR expression (61)(62)(63)(64)(65)(66)(67). In our study, we specifically procured and evaluated a purified population of epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

miR-323a-3p regulates lung fibrosis by targeting multiple profibrotic pathways

Ge¹,

Habiel²,

Hansbro³

et al. 2016

JCI Insight

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“…NR3B1 regulates anti-inflammatory macrophage function by inducing Tnfaip3 transcription and controlling metabolic reprogramming in macrophages. IL-4 and IL-13 have also been shown to induce miR-142-5p and downregulate miR-130a-3p in macrophages, which sustains Stat6 activation and pro-fibrotic gene expression (Su et al, 2015). Finally, N-3 polyunsaturated fatty acids, which exhibit substantial anti-inflammatory in vivo , confer important cardio protective effects by inhibiting macrophage-mediated activation of cardiac fibroblasts.…”

Section: Protective Roles For Anti-inflammatory and Anti-fibrotic Macmentioning

confidence: 99%

Macrophages in Tissue Repair, Regeneration, and Fibrosis

2016

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Inflammatory monocytes and resident tissue macrophages are key regulators of tissue repair, regeneration, and fibrosis. Following tissue injury, monocytes and macrophages undergo marked phenotypic and functional changes to play critical roles during the initiation, maintenance, and resolution phases of tissue repair. Disturbances in macrophage function can lead to aberrant repair, with uncontrolled inflammatory mediator and growth factor production, deficient generation of anti-inflammatory macrophages, or failed communication between macrophages and epithelial cells, endothelial cells, fibroblasts, and stem or tissue progenitor cells all contributing to a state of persistent injury, which may lead to the development of pathological fibrosis. In this review, we discuss the mechanisms that instruct macrophages to adopt pro-inflammatory, pro-wound healing, pro-fibrotic, anti-inflammatory, anti-fibrotic, pro-resolving, and tissue regenerating phenotypes following injury, and highlight how some of these mechanisms and macrophage activation states could be exploited therapeutically.

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miR-142-5p and miR-130a-3p are regulated by IL-4 and IL-13 and control profibrogenic macrophage program

Cited by 220 publications

References 60 publications

Nanoparticle delivery of miR-223 to attenuate macrophage fusion

Nanoparticle delivery of miR-223 to attenuate macrophage fusion

miR-323a-3p regulates lung fibrosis by targeting multiple profibrotic pathways

Macrophages in Tissue Repair, Regeneration, and Fibrosis

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