MiR-26a-5p from HucMSC-derived extracellular vesicles inhibits epithelial mesenchymal transition by targeting Adam17 in silica-induced lung fibrosis

Zhao, Jing; Jiang, Qiyue; Xu, Chunjie; Jia, Qiyue; Wang, Hongwei; Xue, Wenming; Wang, Yan; Zhu, Zhaohui; Lin, Tian

doi:10.1016/j.ecoenv.2023.114950

Cited by 14 publications

(6 citation statements)

References 40 publications

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“…Published role Reference miR-10a-5p Inhibits autoimmune T-cell responses [71] miR-19b-3p a) Increases innate immune response including TLR4 [72,73] miR-23b-3p Reduces cardiomyopathy by targeting/ reducing MyD88-induced NF𝜅B [74,75] miR-26a-5p Reduces fibrosis in lung, reduced in DCM patients and protects heart in animal model [76,77] miR-30a-5p Increased with CVB3 infection, protects against CVB3 myocarditis [78][79][80] miR-31-5p Targets CD40L and SAP to prevent activation of T helper cells [81] miR-99b-5p Inhibits NLRP3 inflammasome, inhibits PI3K/AKT/mTOR signaling [82,83] miR-125b-5p Associated with a number of cardiovascular diseases, but shown to inhibit IL-1𝛽 by targeting TRAF6/MAPK/NF𝜅B signaling [84][85][86][87] miR-143-3p Decreases TLR4, MyD88, and NF𝜅B and increases IL-10 [88] miR-145-5p Decreases TLR4 and PI3K/AKT/mTOR signaling [89,90] miR-148a-3p Inhibits IL-1𝛽 damaging effects and is inhibited by IL-1𝛽, inhibits NF-𝜅B during acute viral myocarditis [91,92] miR-148b-3p Increases proliferation of MSCs and Th2 responses that inhibit TLR4 [93,94] miR-152-3p Decreases PI3K/AKT signaling, inhibits mitochondrial autophagy [95,96] miR-186-5p Increases anti-viral beta-defensin-1 [97] miR-208b-3p Biomarker of sudden cardiac death, but fibroblasts treated with this miR when implanted in myocardial infarcts regenerated the heart and improved cardiac function [98,99] miR-339-5p Targets NEAT1 which regulates innate immune function [100,101] miR-345-5p Targets Drp1 and induces mitochondrial fission, decreases fibrosis by targeting HIF1a [77,102] miR-486-5p Increased with viral infections, but antiviral role…”

Section: Human Mirmentioning

confidence: 99%

“…Interestingly, several of these miRs have already been tested in CVB3 infection, CVB3 myocarditis models, and cardiomyopathy/DCM (Table 1 and Figure 16). [74,[76][77][78]80,91] It is not surprising that an miR associated with CVB3 infection would be detected in EVs from platelets from normal, healthy individuals because this virus is endemic throughout the world and symptoms are typically mild and present often similar to the common cold. [123] Importantly, the viral strain used to induce myocarditis in this model comes from humans rather than animals because CVB3 is one of the rare viruses with no species barrier; so, an miR associated with human CVB3 infection would be expected to reduce viral infection in this model.…”

Section: Human Mirmentioning

confidence: 99%

See 1 more Smart Citation

Reconstituted Extracellular Vesicles from Human Platelets Decrease Viral Myocarditis in Mice

Beetler,

Bruno,

Watkins

et al. 2023

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Patients with viral myocarditis are at risk of sudden death and may progress to dilated cardiomyopathy (DCM). Currently, no disease‐specific therapies exist to treat viral myocarditis. Here it is examined whether reconstituted, lyophilized extracellular vesicles (EVs) from platelets from healthy men and women reduce acute or chronic myocarditis in male mice. Human‐platelet‐derived EVs (PEV) do not cause toxicity, damage, or inflammation in naïve mice. PEV administered during the innate immune response significantly reduces myocarditis with fewer epidermal growth factor (EGF)‐like module‐containing mucin‐like hormone receptor‐like 1 (F4/80) macrophages, T cells (cluster of differentiation molecules 4 and 8, CD4 and CD8), and mast cells, and improved cardiac function. Innate immune mediators known to increase myocarditis are decreased by innate PEV treatment including Toll‐like receptor (TLR)4 and complement. PEV also significantly reduces perivascular fibrosis and remodeling including interleukin 1 beta (IL‐1β), transforming growth factor‐beta 1, matrix metalloproteinase, collagen genes, and mast cell degranulation. PEV given at days 7–9 after infection reduces myocarditis and improves cardiac function. MicroRNA (miR) sequencing reveals that PEV contains miRs that decrease viral replication, TLR4 signaling, and T‐cell activation. These data show that EVs from the platelets of healthy individuals can significantly reduce myocarditis and improve cardiac function.

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Section: Human Mirmentioning

confidence: 99%

Section: Human Mirmentioning

confidence: 99%

Reconstituted Extracellular Vesicles from Human Platelets Decrease Viral Myocarditis in Mice

Beetler,

Bruno,

Watkins

et al. 2023

Small

View full text Add to dashboard Cite

show abstract

“…Engineered MSC-exos can also alleviate lung epithelial-mesenchymal transition (EMT) during pulmonary fibrosis. In related studies, modified HucMSCs-EVs expressing the miR-26a-5p lentivirus could inhibit the Adam17/Notch signalling pathway in MLE-12 cells, thereby improving EMT in silica-induced pulmonary fibrosis [ 70 ]. This suggests that engineered MSCs can affect pulmonary fibrosis by inhibiting cell transformation.…”

Section: Chronic Lung Diseasesmentioning

confidence: 99%

Advancements in engineered mesenchymal stem cell exosomes for chronic lung disease treatment

Zhai,

Cui,

Chen

et al. 2023

J Transl Med

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Chronic lung diseases include an array of conditions that impact airways and lung structures, leading to considerable societal burdens. Mesenchymal stem cells (MSCs) and their exosomes (MSC-exos) can be used for cell therapy and exhibit a diverse spectrum of anti-inflammatory, antifibrotic, and immunomodulatory properties. Engineered MSC-exos possesses enhanced capabilities for targeted drug delivery, resulting in more potent targeting effects. Through various engineering modifications, these exosomes can exert many biological effects, resulting in specific therapeutic outcomes for many diseases. Moreover, engineered stem cell exosomes may exhibit an increased capacity to traverse physiological barriers and infiltrate protected lesions, thereby exerting their therapeutic effects. These characteristics render them a promising therapeutic agent for chronic pulmonary diseases. This article discusses and reviews the strategies and mechanisms of engineered MSC-exos in the treatment of chronic respiratory diseases based on many studies to provide new solutions for these diseases.

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“…The inhibitory effect of miR-1297 on cancer progression has been observed in various malignant entities [113][114][115][116][117][118][119][120][121][122][123][124]. In addition to its role in tumorigenesis, miR-26a-5p similarly plays an important role in pulmonary fibrosis [125] and Alzheimer's disease [126]. However, the included studies provided new information on the role of miR-1297 and miR-26a-5p concerning the pathogenesis of cholesteatoma.…”

Section: Microrna-802mentioning

confidence: 99%

Expression and Regulatory Mechanisms of MicroRNA in Cholesteatoma: A Systematic Review

Dżaman,

Czerwaty,

Reichert

et al. 2023

IJMS

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Cholesteatoma is a temporal bone disease characterized by dysfunctions of keratinocytes. MicroRNAs (miRNAs) are evolutionary conserved noncoding RNAs that regulate mRNA expression. They can be packaged into exosomes and transported to target cells that can be used in the future therapy of cholesteatoma. This study aimed to collect knowledge on the role of miRNAs and exosomal miRNAs in cholesteatoma and was conducted according to the PRISMA guidelines for systematic reviews. Four databases were screened: Pubmed/MEDLINE, Web of Science, Scopus, and the Cochrane Library. The last search was run on the 6th of June 2023. We included full-text original studies written in English, which examined miRNAs in cholesteatoma. The risk of bias was assessed using the Office of Health Assessment and Translation (OHAT) Risk of Bias Rating Tool, modified for the needs of this review. We identified 118 records and included 18 articles. Analyses revealed the downregulation of exosomal miR-17 as well as miR-10a-5p, miR-125b, miR-142-5p, miR34a, miR-203a, and miR-152-5p and the overexpression of exosomal miR-106b-5p as well as miR-1297, miR-26a-5p, miR-199a, miR-508-3p, miR-21-3p, miR-584-5p, and miR-16-1-3p in cholesteatoma. The role of differentially expressed miRNAs in cholesteatoma, including cell proliferation, apoptosis, the cell cycle, differentiation, bone resorption, and the remodeling process, was confirmed, making them a potential therapeutic target in this disease.

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MiR-26a-5p from HucMSC-derived extracellular vesicles inhibits epithelial mesenchymal transition by targeting Adam17 in silica-induced lung fibrosis

Cited by 14 publications

References 40 publications

Reconstituted Extracellular Vesicles from Human Platelets Decrease Viral Myocarditis in Mice

Reconstituted Extracellular Vesicles from Human Platelets Decrease Viral Myocarditis in Mice

Advancements in engineered mesenchymal stem cell exosomes for chronic lung disease treatment

Expression and Regulatory Mechanisms of MicroRNA in Cholesteatoma: A Systematic Review

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