Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/37495
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dc.contributor.authorVAN DEN BROEK, Bram-
dc.contributor.authorWuyts, Charlotte-
dc.contributor.authorSisto, Angela-
dc.contributor.authorPintelon, Isabel-
dc.contributor.authorTimmermans, Jean-Pierre-
dc.contributor.authorSOMERS, Veerle-
dc.contributor.authorTimmerman, Vincent-
dc.contributor.authorHELLINGS, Niels-
dc.contributor.authorIROBI, Joy-
dc.date.accessioned2022-06-13T07:28:27Z-
dc.date.available2022-06-13T07:28:27Z-
dc.date.issued2022-
dc.date.submitted2022-05-19T09:07:32Z-
dc.identifier.citationCell Communication and Signaling, 20 (1) (Art N° 58)-
dc.identifier.issn-
dc.identifier.urihttp://hdl.handle.net/1942/37495-
dc.description.abstractBackground: The contribution of native or modified oligodendroglia-derived extracellular vesicles (OL-EVs) in controlling chronic inflammation is poorly understood. In activated microglia, OL-EVs contribute to the removal of cytotoxic proteins following a proteotoxic stress. Intracellular small heat shock protein B8 (HSPB8) sustain this function by facilitating autophagy and protecting cells against oxidative stress mediated cell death. Therefore, secretion of HSPB8 in OL-EVs could be beneficial for neurons during chronic inflammation. However, how secreted HSPB8 contribute to cellular proteostasis remains to be elucidated. Methods: We produced oligodendroglia-derived EVs, either native (OL-EVs) or HSPB8 modified (OL-HSPB8-EVs), to investigate their effects in controlling chronic inflammation and cellular homeostasis. We analyzed the impact of both EV subsets on either a resting or activated microglial cell line and on primary mixed neural cell culture cells. Cells were activated by stimulating with either tumor necrosis factor-alpha and interleukin 1-beta or with phorbol-12-myristate-13-acetate. Results: We show that OL-EVs and modified OL-HSPB8-EVs are internalized by C20 microglia and by primary mixed neural cells. The cellular uptake of OL-HSPB8-EVs increases the endogenous HSPB8 mRNA expression. Consistently, our results revealed that both EV subsets maintained cellular homeostasis during chronic inflammation with an increase in the formation of autophagic vesicles. Both EV subsets conveyed LC3B-II and BAG3 autophagy markers with an enhanced effect observed for OL-HSPB8-EVs. Moreover, stimulation with either native or modified OL-HSPB8-EVs showed a significant reduction in ubiquitinated protein, reactive oxygen species and mitochondrial depolarization, with OL-HSPB8-EVs exhibiting a more protective effect. Both EV subsets did not induce cell death in the C20 microglia cell line or the primary mixed neural cultures. Conclusion: We demonstrate that the functions of oligodendroglia secreted EVs enriched with HSPB8 have a supportive role, comparable to the native OL-EVs. Further development of engineered oligodendroglia derived EVs could be a novel therapeutic strategy in countering chronic inflammation.-
dc.description.sponsorshipThis work was co-fnanced by the EU through the Interreg IV Flanders—the Netherlands project Interreg V Flanders—the Netherlands project Trans Tech Diagnostics (TTD). In part supported by the Fund for Scientifc Research (FWOFlanders, grant n° G040821N to V.T.) and the University of Antwerp (GOA-BOF grant n° 41667 to V.T.). A.S. holds a Ph.D. fellowship from FWO-Flanders, Belgium. V.T. and J-P.T. are members of the µNeuro Center of Excellence at the University of Antwerp The authors thank Alvarez-Carbonell D, Vanmierlo T, Schepers M, Van Veggel L, Kessels S, Sterck K, De Rijck D, Theuns E, De Winter V, Vanhoof J, Jans M, and Michiels L. for helpful technical assistance and discussions.-
dc.language.isoen-
dc.publisherBMC-
dc.rightsThe Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativeco mmons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.-
dc.subject.otherCNS-
dc.subject.otherEngineered nanocarriers-
dc.subject.otherExtracellular vesicles-
dc.subject.otherMicroglia-
dc.subject.otherMolecular chaperones-
dc.subject.otherCellular inflammation-
dc.subject.otherOligodendroglia-
dc.subject.otherSmall heat shock protein 8-
dc.titleOligodendroglia-derived extracellular vesicles activate autophagy via LC3B/BAG3 to protect against oxidative stress with an enhanced effect for HSPB8 enriched vesicles-
dc.typeJournal Contribution-
dc.identifier.issue1-
dc.identifier.volume20-
local.bibliographicCitation.jcatA1-
dc.description.notesIrobi, J (corresponding author), Hasselt Univ, Biomed Res Inst, Dept Immunol & Infect, Hasselt, Belgium.-
dc.description.notesjoy.irobi@uhasselt.be-
local.publisher.placeCAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND-
local.type.refereedRefereed-
local.type.specifiedArticle-
local.bibliographicCitation.artnr58-
dc.identifier.doi10.1186/s12964-022-00863-x-
dc.identifier.isiWOS:000791359300001-
local.provider.typewosris-
local.description.affiliation[Van den Broek, Bram; Wuyts, Charlotte; Somers, Veerle; Hellings, Niels; Irobi, Joy] Hasselt Univ, Biomed Res Inst, Dept Immunol & Infect, Hasselt, Belgium.-
local.description.affiliation[Sisto, Angela; Timmerman, Vincent] Inst Born Bunge, Dept Biomed Sci, Peripheral Neuropathy Res Grp, Antwerp, Belgium.-
local.description.affiliation[Sisto, Angela; Timmerman, Vincent] Univ Antwerp, Antwerp, Belgium.-
local.description.affiliation[Pintelon, Isabel; Timmermans, Jean-Pierre] Univ Antwerp, Antwerp Ctr Adv Microscopy ACAM, Lab Cell Biol & Histol, Antwerp, Belgium.-
local.uhasselt.internationalno-
item.contributorVAN DEN BROEK, Bram-
item.contributorWuyts, Charlotte-
item.contributorSisto, Angela-
item.contributorPintelon, Isabel-
item.contributorTimmermans, Jean-Pierre-
item.contributorSOMERS, Veerle-
item.contributorTimmerman, Vincent-
item.contributorHELLINGS, Niels-
item.contributorIROBI, Joy-
item.fulltextWith Fulltext-
item.validationecoom 2023-
item.fullcitationVAN DEN BROEK, Bram; Wuyts, Charlotte; Sisto, Angela; Pintelon, Isabel; Timmermans, Jean-Pierre; SOMERS, Veerle; Timmerman, Vincent; HELLINGS, Niels & IROBI, Joy (2022) Oligodendroglia-derived extracellular vesicles activate autophagy via LC3B/BAG3 to protect against oxidative stress with an enhanced effect for HSPB8 enriched vesicles. In: Cell Communication and Signaling, 20 (1) (Art N° 58).-
item.accessRightsOpen Access-
crisitem.journal.eissn1478-811X-
Appears in Collections:Research publications
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