2020
DOI: 10.1111/jcmm.16119
|View full text |Cite
|
Sign up to set email alerts
|

Extracellular vesicles‐derived miR‐150‐5p secreted by adipose‐derived mesenchymal stem cells inhibits CXCL1 expression to attenuate hepatic fibrosis

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
18
0
1

Year Published

2021
2021
2024
2024

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 44 publications
(26 citation statements)
references
References 43 publications
0
18
0
1
Order By: Relevance
“…EVs from AD-MSC engineered to over-produce miR-122 (a known inhibitor of fibrosis) suppressed proliferation and collagen production in activated human or mouse HSC with suppressed expression of P4HA1 , IGF-1R and CCNG1 target genes [ 275 ]. Administration of miR-122-enriched AD-MSC EVs in CCl 4 -treated mice resulted in attenuation of hepatic fibrosis, suppression of hepatic TGF-β1 and αSMA expression, and inhibition of serum ALT, hyaluronan, type III procollagen, aspartate transaminase and liver hydroxyproline [ 275 ] while mir-150-5p-enriched AD-MSC EVs were anti-fibrotic due to targeting of CXCL1 [ 276 ]. Similarly, EVs from miR-181-5p-over-expressing AD-MSCs were antifibrogenic in vitro and anti-fibrotic in vivo at least in part due to down regulation of STAT3 and Bcl2 , stimulation of autophagy, and suppression of fibrogenic gene expression [ 277 ].…”
Section: Hepatic Fibrosismentioning
confidence: 99%
“…EVs from AD-MSC engineered to over-produce miR-122 (a known inhibitor of fibrosis) suppressed proliferation and collagen production in activated human or mouse HSC with suppressed expression of P4HA1 , IGF-1R and CCNG1 target genes [ 275 ]. Administration of miR-122-enriched AD-MSC EVs in CCl 4 -treated mice resulted in attenuation of hepatic fibrosis, suppression of hepatic TGF-β1 and αSMA expression, and inhibition of serum ALT, hyaluronan, type III procollagen, aspartate transaminase and liver hydroxyproline [ 275 ] while mir-150-5p-enriched AD-MSC EVs were anti-fibrotic due to targeting of CXCL1 [ 276 ]. Similarly, EVs from miR-181-5p-over-expressing AD-MSCs were antifibrogenic in vitro and anti-fibrotic in vivo at least in part due to down regulation of STAT3 and Bcl2 , stimulation of autophagy, and suppression of fibrogenic gene expression [ 277 ].…”
Section: Hepatic Fibrosismentioning
confidence: 99%
“…Anti-oxidative glutathione peroxidase 1 delivered by the MSC-exosomes decreased oxidative stress and increased hepatocyte proliferation in CCl 4 -injured liver [ 145 ]. Furthermore, the treatment of MSCs-EV containing miR-150-5p reduced the expression of CXC chemokine-ligand-1, one of the profibrotic chemokines in HSCs, and attenuated liver fibrosis [ 146 ]. The miR-1246 contained in MSC-exosomes was shown to protect hepatocytes from ischemia-reperfusion injury and modulate the balance of regulatory T cells and Th17 cells to suppress inflammation and maintain immune tolerance [ 147 ].…”
Section: Msc Cell-free Therapy For Liver Fibrosismentioning
confidence: 99%
“…Micro RNAs (miRNAs, or miRs) are small non-coding RNA molecules (about 22 nucleotides) that change gene expression at the post-transcriptional level, leading to changes in protein synthesis. MiR-150 is a representative anti-fibrotic miRNA, which can inhibit the activation of hepatic stellate cells through the inhibition of C-X-C motif chemokine ligand 1 (CXCL1), and is a natural component of ASCs EVs[ 35 ]. Paik et al [ 36 ] transfected ASCs with miR-150 to explore whether additional miR-150 secretion could boost the anti-fibrotic ability.…”
Section: Ways To Enhance Ascs Therapeutic Performancementioning
confidence: 99%