Exosomes derived from mesenchymal stem cells attenuate the progression of atherosclerosis in ApoE−/- mice via miR-let7 mediated infiltration and polarization of M2 macrophage

Li, Jiangbing; Xue, Hao; Li, Tingting; Chu, Xili; Xin, Danqing; Xiong, Ye; Qiu, Wei; Gao, Xiao; Qian, Mingyu; Xu, Jiangye; Wang, Zhen; Li, Gang

doi:10.1016/j.bbrc.2019.02.005

Cited by 157 publications

(111 citation statements)

References 38 publications

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“…The inhibitory effects of exosomes on B‐lymphocyte proliferation as well as B‐cell function were also observed, which was through the alteration of relevant mRNA levels, such as CXCL8 and MZB1 84 . It was demonstrated that MSC‐derived exosomes could suppress M1 macrophage function, while directly increasing M2 polarization through the activation of the miR‐let7/HMGA2/NF‐κB pathway 85 . CCR2 on MSC‐derived exosomes was also involved in polarization from M1 to M2 through the activation of the CCL2/CCR2 axis 86 .…”

Section: Introductionmentioning

confidence: 95%

Biology and therapeutic potential of mesenchymal stem cell‐derived exosomes

2020

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Mesenchymal stem cells (MSC) are multipotent stromal cells with the potential to differentiate into several cell types. MSC‐based therapy has emerged as a promising strategy for various diseases. Accumulating evidence suggests that the paracrine effects of MSC are partially exerted by the secretion of soluble factors, in particular exosomes. MSC‐derived exosomes are involved in intercellular communication through transfer of proteins, RNA, DNA and bioactive lipids, which might constitute a novel intercellular communication mode. This review illustrates the current knowledge on the composition and biological functions as well as the therapeutic potential of MSC‐derived exosomes in cancer, with a focus on clinical translation opportunities.

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Section: Introductionmentioning

confidence: 95%

Biology and therapeutic potential of mesenchymal stem cell‐derived exosomes

2020

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“…13) In addition, HMGA2 was discovered to be involved in the development and progression of many cardiovascular diseases, such as atherosclerosis, intravenous leiomyomatosis, and cardiac lipomas. [14][15][16] Moreover, Belge et al found that HMGA2 was over-expressed in acute aortic dissection and associated with endothelial-mesenchymal transition. 17) However, the biological function of HMGA2 in TAAD pathogenesis and whether it was regulated by miR-26b has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

MiR-26b Suppresses the Development of Stanford Type A Aortic Dissection by Regulating HMGA2 and TGF-β/Smad3 Signaling Pathway

Yang

Wu²,

Liu

et al. 2020

ATCS

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Purpose: Stanford type A aortic dissection (TAAD) is one of the most dangerous cardiovascular diseases. MicroRNAs (miRNAs) have been considered as potential therapeutic targets for TAAD. In this present study, we aimed to investigate the functional role and regulatory mechanism of miR-26b in TAAD development. Materials and Methods: MiR-26b mRNA expression was detected by real-time polymerase chain reaction (RT-PCR) and protein levels were measured by Western blot. Verifying the direct target of miR-26b was used by dual luciferase assay, RT-PCR, and Western blot. Cell Counting Kit-8 (CCK-8) and TUNEL staining assays were applied for detecting rat aortic vascular smooth muscle cells (VSMCs) viability and apoptosis, respectively. Results: We found that miR-26b was under-expressed in TAAD patients and closely associated with the poor prognosis of TAAD patients. Re-expression of miR-26b facilitated while knockdown of miR-26b inhibited VSMC proliferation. However, miR-26b showed the opposite effect on cell apoptosis. More importantly, high-mobility group AT-hook 2 (HMGA2) was verified as the direct target of miR-26b. Furthermore, transforming growth factor beta (TGF-β)/Smad3 signaling pathway was involved in the development of TAAD modulated by miR-26b. Conclusion: miR-26b impeded TAAD development by regulating HMGA2 and TGF-β/ Smad3 signaling pathway, which provided a potential biomarker for TAAD treatment.

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“…[ 31 ] Here, we focused on the comparison of miRNA profiles among PMSC‐NVs, MSC‐NVs, and PMSC as internal components, owing to their abundance in exosomes [ 32 ] and reported anti‐atherogenic paracrine effect. [ 33 ] MSC‐derived exosomes [ 34 ] contain miRNAs with anti‐inflammatory (miR‐21, [ 35 ] miR‐let7, [ 34 ] miR‐126, [ 36 ] miR‐145, [ 37 ] and miR‐146 [ 38 ] ), pro‐EC recovery (miR‐126 [ 39 ] and miR‐146 [ 40 ] ), and anti‐VSMC activation (miR‐143 [ 32 ] and miR‐145 [ 32,37 ] ) miRNAs. The internal components of NVs were preserved in a significant degree from the corresponding hMSC source (Figure 1I).…”

Section: Discussionmentioning

confidence: 99%

Anti‐Atherogenic Effect of Stem Cell Nanovesicles Targeting Disturbed Flow Sites

Yoon

Kim

Kang

et al. 2020

Small

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Atherosclerosis development leads to irreversible cascades, highlighting the unmet need for improved methods of early diagnosis and prevention. Disturbed flow formation is one of the earliest atherogenic events, resulting in increased endothelial permeability and subsequent monocyte recruitment. Here, a mesenchymal stem cell (MSC)‐derived nanovesicle (NV) that can target disturbed flow sites with the peptide GSPREYTSYMPH (PREY) (PMSC‐NVs) is presented which is selected through phage display screening of a hundred million peptides. The PMSC‐NVs are effectively produced from human MSCs (hMSCs) using plasmid DNA designed to functionalize the cell membrane with PREY. The potent anti‐inflammatory and pro‐endothelial recovery effects are confirmed, similar to those of hMSCs, employing mouse and porcine partial carotid artery ligation models as well as a microfluidic disturbed flow model with human carotid artery‐derived endothelial cells. This nanoscale platform is expected to contribute to the development of new theragnostic strategies for preventing the progression of atherosclerosis.

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Exosomes derived from mesenchymal stem cells attenuate the progression of atherosclerosis in ApoE−/- mice via miR-let7 mediated infiltration and polarization of M2 macrophage

Cited by 157 publications

References 38 publications

Biology and therapeutic potential of mesenchymal stem cell‐derived exosomes

Biology and therapeutic potential of mesenchymal stem cell‐derived exosomes

MiR-26b Suppresses the Development of Stanford Type A Aortic Dissection by Regulating HMGA2 and TGF-β/Smad3 Signaling Pathway

Anti‐Atherogenic Effect of Stem Cell Nanovesicles Targeting Disturbed Flow Sites

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