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dc.contributor.authorMomen-Heravi, Fatemeh
dc.contributor.authorBala, Shashi
dc.contributor.authorBukong, Terence N.
dc.contributor.authorSzabo, Gyongyi
dc.date2022-08-11T08:08:37.000
dc.date.accessioned2022-08-23T16:01:14Z
dc.date.available2022-08-23T16:01:14Z
dc.date.issued2014-03-29
dc.date.submitted2014-09-11
dc.identifier.citationNanomedicine. 2014 Mar 29. doi: 10.1016/j.nano.2014.03.014 <a href="http://dx.doi.org/10.1016/j.nano.2014.03.014">Link to article on publisher's site</a>
dc.identifier.issn1549-9634 (Linking)
dc.identifier.doi10.1016/j.nano.2014.03.014
dc.identifier.pmid24685946
dc.identifier.urihttp://hdl.handle.net/20.500.14038/31074
dc.description.abstractExosomes, membranous nanovesicles, naturally carry bio-macromolecules and play pivotal roles in both physiological intercellular crosstalk and disease pathogenesis. Here, we showed that B cell-derived exosomes can function as vehicles to deliver exogenous miRNA-155 mimic or inhibitor into hepatocytes or macrophages, respectively. Stimulation of B cells significantly increased exosome production. Unlike in parental cells, baseline level of miRNA-155 was very low in exosomes derived from stimulated B cells. Exosomes loaded with a miRNA-155 mimic significantly increased miRNA-155 levels in primary mouse hepatocytes and the liver of miRNA-155 knockout mice. Treatment of RAW macrophages with miRNA-155 inhibitor loaded exosomes resulted in statistically significant reduction in LPS-induced TNFalpha production and partially prevented LPS-induced decrease in SOCS1 mRNA levels. Furthermore, exosome-mediated miRNA-155 inhibitor delivery resulted in functionally more efficient inhibition and less cellular toxicity compared to conventional transfection methods. Similar approaches could be useful in modification of target biomolecules in vitro and in vivo.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24685946&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.nano.2014.03.014
dc.subjectCell Biology
dc.subjectDigestive System Diseases
dc.subjectGastroenterology
dc.subjectGenomics
dc.subjectHepatology
dc.subjectImmunopathology
dc.subjectNanomedicine
dc.titleExosome-mediated delivery of functionally active miRNA-155 inhibitor to macrophages
dc.typeJournal Article
dc.source.journaltitleNanomedicine : nanotechnology, biology, and medicine
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gastroenterology_pp/130
dc.identifier.contextkey6105455
html.description.abstract<p>Exosomes, membranous nanovesicles, naturally carry bio-macromolecules and play pivotal roles in both physiological intercellular crosstalk and disease pathogenesis. Here, we showed that B cell-derived exosomes can function as vehicles to deliver exogenous miRNA-155 mimic or inhibitor into hepatocytes or macrophages, respectively. Stimulation of B cells significantly increased exosome production. Unlike in parental cells, baseline level of miRNA-155 was very low in exosomes derived from stimulated B cells. Exosomes loaded with a miRNA-155 mimic significantly increased miRNA-155 levels in primary mouse hepatocytes and the liver of miRNA-155 knockout mice. Treatment of RAW macrophages with miRNA-155 inhibitor loaded exosomes resulted in statistically significant reduction in LPS-induced TNFalpha production and partially prevented LPS-induced decrease in SOCS1 mRNA levels. Furthermore, exosome-mediated miRNA-155 inhibitor delivery resulted in functionally more efficient inhibition and less cellular toxicity compared to conventional transfection methods. Similar approaches could be useful in modification of target biomolecules in vitro and in vivo.</p>
dc.identifier.submissionpathgastroenterology_pp/130
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology


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