miRNAomics analysis reveals the promoting effects of cigarette smoke extract-treated Beas-2B-derived exosomes on macrophage polarization

Chen, Zhen; Wu, Hao; Shi, Rui; Fan, Weiyang; Zhang, Jiashuo; Sui, Weiwei; Wang, Yonggang; Li, Peibo

doi:10.1016/j.bbrc.2021.07.093

Cited by 22 publications

(18 citation statements)

References 30 publications

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“…In our previous study, we found that CSE promoted M1 macrophage polarization via upregulated EVs miR-21-3p and miR-27b-3p derived from BEAS-2B cells ( 5 ). Thus, we speculated that naringenin suppressed M1 macrophage polarization via downregulating these miRNAs in this study.…”

Section: Resultsmentioning

confidence: 98%

“…The polarization-related surface markers of RAW264.7, MH-S, and THP-1 macrophages were detected by flow cytometry. In our previous study ( 5 ), we found that 10 μg/ml CSE-EVs could significantly promote M1 polarization of RAW264.7 macrophages, thus we treated macrophages (5×10 4 cells/cm 2 ) with 10 μg/mL EVs in EVs-free RPMI 1640 mediums for 24 h in this study. For positive control, 2 μM SF1670 and 1 μM AG14361 were used to inhibit PTEN and PAPR1 expression of THP-1 cells, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Excessive accumulation of M1 macrophages at inflammatory sites can lead to exacerbated tissue damage and more severe inflammatory storms ( 4 ). In our previous study, we found that cigarette smoke extract (CSE) upregulated the human bronchial epithelial cell line (BEAS-2B)-derived EVs miR-21-3p and miR-27b-3p thereby promoting M1 macrophage polarization ( 5 ).…”

Section: Introductionmentioning

confidence: 99%

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Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Chen

Fan

et al. 2022

Front. Immunol.

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Extracellular vesicles (EVs)-mediated epithelium-macrophage crosstalk has been proved to maintain lung homeostasis in cigarette smoke-induced lung diseases such as chronic obstructive pulmonary disease (COPD). In our previous study, we found that EVs derived from cigarette smoke extract (CSE) treated BEAS-2B promoted M1 macrophage polarization, which probably accelerated the development of inflammatory responses. Naringenin has been proved to suppress M1 macrophage polarization, but whether naringenin regulates macrophage polarization mediated by EVs has not been reported. In this study, we firstly found that EVs derived from naringenin and CSE co-treated BEAS-2B significantly inhibited the expression of CD86 and CD80 and the secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS), and IL-12 in macrophage induced by EVs derived from CSE-treated BEAS-2B. Further research revealed that naringenin downregulated BEAS-2B-derived EVs miR-21-3p which targeted phosphatase and tensin homolog deleted on chromosome ten/protein kinase B (PTEN/AKT) cascade in macrophages and then suppressed M1 macrophage polarization. Subsequent proteomics suggested that naringenin decreased BEAS-2B-derived EVs poly ADP-ribose polymerase (PARP)1 expression thereby suppressing M1 macrophage polarization probably. Our study provides novel pharmacological references for the mechanism of naringenin in the treatment of cigarette smoke-induced lung inflammatory diseases.

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Section: Resultsmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Chen

Fan

et al. 2022

Front. Immunol.

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“…Adipose-derived mesenchymal stem cell-derived exosomes promote macrophage polarization by inhibiting TLR4 and alleviating lung injury ( 43 ). Previous studies have demonstrated that alveolar epithelial-derived exosomes also mediate macrophage activation ( 29 , 44 ). These results indicate that exosomes play a critical role in AM activation.…”

Section: Discussionmentioning

confidence: 99%

Epithelial‑derived exosomes promote M2 macrophage polarization via Notch2/SOCS1 during mechanical ventilation

et al. 2022

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Alveolar macrophages (AMs) play an essential role in ventilator-induced lung injury (VILI). Exosomes and their cargo, including microRNAs (miRNAs/miRs) serve as regulators of the intercellular communications between macrophages and epithelial cells (ECs), and are involved in maintaining homeostasis in lung tissue. The present study found that exosomes released by ECs subjected to cyclic stretching promoted M2 macrophage polarization. It was demonstrated that miR-21a-5p, upregulated in epithelial-derived exosomes, increased the percentage of M2 macrophages by suppressing the expression of Notch2 and the suppressor of cytokine signaling 1 (SOCS1). The overexpression of Notch2 decreased the percentage of M2 macrophages. However, these effects were reversed by the downregulation of SOCS1. The percentage of M2 macrophages was increased in both short-term high- and low-tidal-volume mechanical ventilation, and the administration of exosomes-derived from cyclically stretched ECs had the same function. However, the administration of miR-21a-5p antagomir decreased M2 macrophage activation induced by cyclically stretched ECs or ventilation. Thus, the present study demonstrates that the intercellular transferring of exosomes from ECs to AMs promotes M2 macrophage polarization. Exosomes may prove to be a novel treatment for VILI.

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“…The human bronchial epithelial BEAS-2B cell line exposed to various factors secreted exosomes containing miRNAs into the extracellular space [ 54 , 55 ]. Recently, Chen et al found that exosomes derived from BEAS-2B cell treated with cigarette smoke extract lead to RAW264.7 macrophages polarization by increasing the percentages of CD86 + , CD80 + , CD163 + , and CD206 + cells, but also the secretion of TNF-α, IL-6, iNOS, IL-10, Arg-1, and TGF-β [ 56 ]. Exosomes derived from lung epithelium may be used to develop biomarkers for diagnosing and treating cigarette smoke-related lung diseases.…”

Section: Mirnas As Biomarkersmentioning

confidence: 99%

The role of miRNAs in alveolar epithelial cells in emphysema

Hayek

Kośmider

Bahmed

2021

Biomedicine & Pharmacotherapy

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miRNAomics analysis reveals the promoting effects of cigarette smoke extract-treated Beas-2B-derived exosomes on macrophage polarization

Cited by 22 publications

References 30 publications

Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Naringenin suppresses BEAS-2B-derived extracellular vesicular cargoes disorder caused by cigarette smoke extract thereby inhibiting M1 macrophage polarization

Epithelial‑derived exosomes promote M2 macrophage polarization via Notch2/SOCS1 during mechanical ventilation

The role of miRNAs in alveolar epithelial cells in emphysema

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