We are analyzing https://link.springer.com/article/10.1007/s12035-022-02833-3.

Title:
MSC Promotes the Secretion of Exosomal miR-34a-5p and Improve Intestinal Barrier Function Through METTL3-Mediated Pre-miR-34A m6A Modification | Molecular Neurobiology
Description:
Intestinal ischemia/reperfusion (I/R) injury (IIRI) is associated with high prevalence and mortality rate. Recently, mesenchymal stem cell (MSC) therapy attracted more attentions. However, the function and regulatory mechanism of MSC-derived exosomal miRNAs during IIRI remain largely uninvestigated. The in vitro and in vivo IIRI models were established. MSC were characterized by immunofluorescent staining and flow cytometry. Purified exosomes were characterized by transmission electron microscopy (TEM), flow cytometry, and western blot. The expression of key molecules was detected by western blot and qRT-PCR. CCK-8, TUNEL, and transepithelial electrical resistance (TER) assays were employed to assess cell viability, apoptosis, and intestinal integrity, respectively. Pre-miR-34A m6 modification was evaluated by methylated RNA immunoprecipitation (MeRIP)-qPCR. RNA pull-down and RIP were used to validate the direct association between pre-miR-34A and IGF2BP3. MSC-derived exosomal miR-34a-5p alleviated OGD/R-induced injury. In addition, MSC ameliorated OGD/R-induced injury through METTL3 pathway. Mechanistic study revealed that miR-34a-5p was modulated by METTL3/IGF2BP3-mediated m6A modification in MSC. The in vitro and in vivo functional experiments revealed that MSC secreted exosomal miR-34a-5p and ameliorated IIRI through METTL3/IGF2BP3-mediated m6A modification of pre-miR-34A. MSC promoted the secretion of exosomal miR-34a-5p and improved intestinal barrier function through METTL3/IGF2BP3-mediated pre-miR-34A m6A modification.
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Keywords {🔍}

pubmed, article, google, scholar, intestinal, cas, central, stem, cell, cells, mesenchymal, rna, barrier, injury, function, msc, modification, ischemiareperfusion, exosomal, mirap, zhang, data, premira, nmethyladenosine, kunming, privacy, cookies, content, research, iiri, mechanism, mscderived, exosomes, expression, access, microrna, regulation, epithelial, methylation, bowel, micrornas, res, chen, biol, httpsdoiorgs, yunnan, project, medical, university, authors,

Topics {✒️}

msc-derived exosomal mir-34a/c-5p mettl3/igf2bp3-mediated m6a modification pre-mir-34a m6 modification ischemia/reperfusion-induced intestinal injury exosomal mir-34a-5p rangtp-dependent dsrna-binding protein msc-derived exosomal mirnas month download article/chapter mesenchymal stem cells intestinal ischemia/reperfusion injury intestinal ischemia-reperfusion injury intestinal ischemia/reperfusion damage mir-34a-5p cytochalasin-induced actin disruption mesenchymal stem cell intestinal epithelial cells pre-mir-34a nucleotide-binding oligomerization domain rna n6-methyladenosine methylation enzyme-linked immunosorbent assay wei-ming li rna-interference enzyme dicer a-igf2bp2-dependent mechanism ischemia/reperfusion injury intestinal mucosal lesion intestinal epithelial claudins intestinal barrier injury n6-methyladenosine mettl3 paraformaldehyde pre-mirnas tnf-alpha-regulated mechanism snail/claudins signaling pathway full article pdf intestinal barrier function ischemia/reperfusion iiri yi-jun li intestinal barrier dysfunction exosome-mediated effects exosome-mediated transfer privacy choices/manage cookies exosomes derived human participants performed repair intestinal barrier barrier function dysregulation transmission electron microscopy transepithelial electrical resistance code availability tight junction disruption inflammatory bowel disease pre-mirnas methylated rna immunoprecipitation

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         headline:MSC Promotes the Secretion of Exosomal miR-34a-5p and Improve Intestinal Barrier Function Through METTL3-Mediated Pre-miR-34A m6A Modification
         description:Intestinal ischemia/reperfusion (I/R) injury (IIRI) is associated with high prevalence and mortality rate. Recently, mesenchymal stem cell (MSC) therapy attracted more attentions. However, the function and regulatory mechanism of MSC-derived exosomal miRNAs during IIRI remain largely uninvestigated. The in vitro and in vivo IIRI models were established. MSC were characterized by immunofluorescent staining and flow cytometry. Purified exosomes were characterized by transmission electron microscopy (TEM), flow cytometry, and western blot. The expression of key molecules was detected by western blot and qRT-PCR. CCK-8, TUNEL, and transepithelial electrical resistance (TER) assays were employed to assess cell viability, apoptosis, and intestinal integrity, respectively. Pre-miR-34A m6 modification was evaluated by methylated RNA immunoprecipitation (MeRIP)-qPCR. RNA pull-down and RIP were used to validate the direct association between pre-miR-34A and IGF2BP3. MSC-derived exosomal miR-34a-5p alleviated OGD/R-induced injury. In addition, MSC ameliorated OGD/R-induced injury through METTL3 pathway. Mechanistic study revealed that miR-34a-5p was modulated by METTL3/IGF2BP3-mediated m6A modification in MSC. The in vitro and in vivo functional experiments revealed that MSC secreted exosomal miR-34a-5p and ameliorated IIRI through METTL3/IGF2BP3-mediated m6A modification of pre-miR-34A. MSC promoted the secretion of exosomal miR-34a-5p and improved intestinal barrier function through METTL3/IGF2BP3-mediated pre-miR-34A m6A modification.
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      description:Intestinal ischemia/reperfusion (I/R) injury (IIRI) is associated with high prevalence and mortality rate. Recently, mesenchymal stem cell (MSC) therapy attracted more attentions. However, the function and regulatory mechanism of MSC-derived exosomal miRNAs during IIRI remain largely uninvestigated. The in vitro and in vivo IIRI models were established. MSC were characterized by immunofluorescent staining and flow cytometry. Purified exosomes were characterized by transmission electron microscopy (TEM), flow cytometry, and western blot. The expression of key molecules was detected by western blot and qRT-PCR. CCK-8, TUNEL, and transepithelial electrical resistance (TER) assays were employed to assess cell viability, apoptosis, and intestinal integrity, respectively. Pre-miR-34A m6 modification was evaluated by methylated RNA immunoprecipitation (MeRIP)-qPCR. RNA pull-down and RIP were used to validate the direct association between pre-miR-34A and IGF2BP3. MSC-derived exosomal miR-34a-5p alleviated OGD/R-induced injury. In addition, MSC ameliorated OGD/R-induced injury through METTL3 pathway. Mechanistic study revealed that miR-34a-5p was modulated by METTL3/IGF2BP3-mediated m6A modification in MSC. The in vitro and in vivo functional experiments revealed that MSC secreted exosomal miR-34a-5p and ameliorated IIRI through METTL3/IGF2BP3-mediated m6A modification of pre-miR-34A. MSC promoted the secretion of exosomal miR-34a-5p and improved intestinal barrier function through METTL3/IGF2BP3-mediated pre-miR-34A m6A modification.
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