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The Therapeutic Effects of Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells on Scleroderma

Yue Yu; Liangliang Shen; Xiaoyun Xie; Jingjun Zhao; Miao Jiang
Tissue Engineering and Regenerative Medicine · Vol. 19, Issue 1 · pp. 141-150 · 2022

Abstract

Background: Scleroderma is a multisystem disease in which tissue fibrosis is caused by inflammation and vascular damage. The mortality of scleroderma has remained high due to a lack of effective treatments. However, exosomes derived from human umbilical cord mesenchymal stem cells (HUMSCs)-Ex have been regarded as potential treatments for various autoimmune diseases, and may also act as candidates for treating scleroderma. Methods: Mice with scleroderma received a single 50 μg HUMSCs-Ex. HUMSCs-Ex was characterized using transmission electron microscopy, nanoparticle tracking analysis and nanoflow cytometry. The therapeutic efficacy was assessed using histopathology, immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay and western blot. Results: HUMSCs-Ex ameliorated the deposition of extracellular matrix and suppressed the epithelial-mesenchymal transition process, and the effects lasted at least three weeks. In addition, HUMSCs-Ex promoted M1 macrophage polarization and inhibited M2 macrophage polarization, leading to the restoration of the balance of M1/M2 macrophages. Conclusion: We investigated the potential antifibrotic and anti-inflammatory effects of HUMSCs-Ex in a bleomycin-induced mouse model of scleroderma. So HUMSCs-Ex could be considered as a candidate therapy for scleroderma.

Bibliographic Information

JournalTissue Engineering and Regenerative Medicine
PublisherSpringer
Publication Date2022-02-01
Publication Year2022
Volume19
Issue1
Pages141-150
Document TypeJournal Article
Print ISSN1738-2696
eISSN2212-5469
DOI10.1007/s13770-021-00405-5

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NARA Access Coverage2012-01-01~Current
Journal Homepagehttps://www.springer.com/journal/13770
Publisher PageOpen Publisher Page
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