We are analyzing https://link.springer.com/article/10.1186/s12951-023-01951-x.

Title:
Human umbilical cord mesenchymal stem cells derived exosome shuttling mir-129-5p attenuates inflammatory bowel disease by inhibiting ferroptosis | Journal of Nanobiotechnology
Description:
Background Ferroptosis, a unique form of non-apoptotic cell death, is dependent on iron and lipoperoxidation, and has been shown to be associated with the pathogenesis of inflammatory bowel disease (IBD). Human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) are involved in cell survival, immune conditioning, and damage repair. However, the relationship between hucMSC-Ex, IBD, and ferroptosis is unknown. This paper explores the role of hucMSC-Ex in the repair of IBD through the regulation of the ferroptosis signaling pathway. Results In this study, we used small RNA sequencing to find that miR-129-5p was highly expressed in hucMSC-Ex, and by predicting its targeting to ACSL4, we verified the effect of miR-129-5p on mice IBD in vitro and human colonic epithelial cells (HCoEpiC) in vivo. We found that miR-129-5p reduces ferroptosis in intestinal epithelial cells by targeting ACSL4 to repair IBD, which provides new strategies for the prevention and treatment of IBD. Conclusion In conclusion, our results demonstrate that hucMSC-Ex relieves IBD by targeting ACSL4 with miR-129-5p to inhibit lipid peroxidation (LPO) and ferroptosis, reducing intestinal inflammation and repairing damages. Graphic abstract Mechanism of hucMSC-Ex inhibiting ferroptosis in intestinal epithelial cells. System Xc− mediates the transport of extracellular cystine into the cell, which gets reduced to cysteine to participate in GSH-mediated metabolism. GPX4 strongly inhibits ferroptosis by helping scavenge reactive oxygen species. The depletion of GSH correlates with decreased GPX4, and the imbalance of the antioxidant system leads to the formation of toxic phospholipid hydroperoxide, which promotes the occurrence of ferroptosis with the participation of irons. HucMSC-Ex has the ability to relieve GSH and GPX4 depletion and repair the intracellular antioxidant system. Ferric ions enter the cytosol through DMT1 and participate in lipid peroxidation. HucMSC-Ex can reduce the expression of DMT1 and alleviate this process. HucMSC-Ex-derived miR-129-5p targets ACSL4 and reduces the expression of ACSL4, an enzyme that mediates the conversion of PUFAs into phospholipids in intestinal epithelial cells, and is a positive regulator of lipid peroxidation. Abbreviations: GSH, glutathione; GPX4, glutathione peroxidase 4; GSSG, oxidized glutathione; DMT1, divalent metal transporter 1; ACSL4, acyl-CoA synthetase long-chain family member 4; PUFAs, polyunsaturated fatty acids; ALOXs, lipoxygenases; CoA, coenzyme A; PL, phospholipid; PLOOH, hydroperoxides, LOH, phospholipid alcohols; LPO, lipid peroxidation.
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Keywords {🔍}

hucmscex, ferroptosis, mice, ibd, mirp, article, pubmed, acsl, expression, cells, google, scholar, group, fig, intestinal, cell, cas, results, colon, inflammatory, mimics, gpx, exosomes, repair, effect, data, iron, tissue, analysis, epithelial, lipid, dss, showed, stem, treatment, lpo, increased, groups, staining, protein, transfection, disease, hcoepic, colitis, mrna, western, significantly, mesenchymal, peroxidation, studies,

Topics {✒️}

mir-378a-5p/nlrp3 axis mesenchymal stem/stromal cells human umbilical cord umbilical cord blood inflammatory bowel disease mesenchymal stem cells alleviate myocardial ischemia/reperfusion lipid peroxidation-derived electrophiles mir-146a/sumo1 axis pro-inflammatory factors tnf-α dual-luciferase reporter gene complex bio-derived vesicle alleviates dss-induced enteritis short-chain rna molecules xu zhang & fei mao inflammatory bowel diseases article download pdf 3t3-l1 adipose cell hucmsc-derived exosomes alleviate gut metagenomics-metabolomics-farnesoid nrf2/ho-1 signaling pathway delivering mir-23a-3p [58] lps-induced inflammatory environment pluripotent stem cells spinal cord injury shuttling mir-182 goat anti-rabbit igg dss-induced mouse models pro-inflammatory factors il-6 human caco-2 cells steady-state metabolic control nf-κb signals identified mir-129-5p contained efficient exosome-based theranostics anti-inflammatory factor il-10 additional 400 µg/ml exosomes carrying mir-129-5p mimics alleviate dss-induced ibd ferroptosis-mediated tissue injury inhibiting nrf2/ho-1 pathway low-density electron component alcoholic liver disease reduces myocardial injury msc-derived exosomes mir-129-5p targets acsl4 emerging cell-free therapy anti-peroxidation mechanism breaks intestinal ischemia/reperfusion mir-182-regulated macrophage polarization extracellular vesicles derived

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            Mesenchymal stem cell-derived exosomes
            Ferroptosis
            miR-129-5p
            Inflammatory bowel disease
            ACSL4
            Lipid peroxidation
            Biotechnology
            Nanotechnology
            Molecular Medicine
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         miR-129-5p
         Inflammatory bowel disease
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         Lipid peroxidation
         Biotechnology
         Nanotechnology
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