Matches in SemOpenAlex for { <https://semopenalex.org/work/W4229058663> ?p ?o ?g. }
- W4229058663 abstract "Abstract Background 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." @default.
- W4229058663 created "2022-05-08" @default.
- W4229058663 creator A5000437761 @default.
- W4229058663 creator A5008950728 @default.
- W4229058663 creator A5009656164 @default.
- W4229058663 creator A5031340408 @default.
- W4229058663 creator A5035053042 @default.
- W4229058663 creator A5047281271 @default.
- W4229058663 creator A5051450048 @default.
- W4229058663 creator A5065437335 @default.
- W4229058663 creator A5085832818 @default.
- W4229058663 date "2022-05-05" @default.
- W4229058663 modified "2023-10-16" @default.
- W4229058663 title "Oligodendroglia-derived extracellular vesicles activate autophagy via LC3B/BAG3 to protect against oxidative stress with an enhanced effect for HSPB8 enriched vesicles" @default.
- W4229058663 cites W1594293927 @default.
- W4229058663 cites W180867511 @default.
- W4229058663 cites W1965891907 @default.
- W4229058663 cites W1977709885 @default.
- W4229058663 cites W1990388063 @default.
- W4229058663 cites W1994516064 @default.
- W4229058663 cites W1994696929 @default.
- W4229058663 cites W2008219352 @default.
- W4229058663 cites W2014610992 @default.
- W4229058663 cites W2020863352 @default.
- W4229058663 cites W2025665129 @default.
- W4229058663 cites W2051784879 @default.
- W4229058663 cites W2059895668 @default.
- W4229058663 cites W2076104235 @default.
- W4229058663 cites W2079013802 @default.
- W4229058663 cites W2086612059 @default.
- W4229058663 cites W2094510532 @default.
- W4229058663 cites W2126805358 @default.
- W4229058663 cites W2131007152 @default.
- W4229058663 cites W2158621084 @default.
- W4229058663 cites W2166846320 @default.
- W4229058663 cites W2171529323 @default.
- W4229058663 cites W2237695503 @default.
- W4229058663 cites W2278678564 @default.
- W4229058663 cites W2279983710 @default.
- W4229058663 cites W2524223359 @default.
- W4229058663 cites W2553902009 @default.
- W4229058663 cites W2602035017 @default.
- W4229058663 cites W2735590725 @default.
- W4229058663 cites W2763145678 @default.
- W4229058663 cites W2782358406 @default.
- W4229058663 cites W2796493184 @default.
- W4229058663 cites W2796631501 @default.
- W4229058663 cites W2884031535 @default.
- W4229058663 cites W2900600199 @default.
- W4229058663 cites W2900756811 @default.
- W4229058663 cites W2911703946 @default.
- W4229058663 cites W2962463215 @default.
- W4229058663 cites W2964104709 @default.
- W4229058663 cites W2964677741 @default.
- W4229058663 cites W2964684793 @default.
- W4229058663 cites W2976515727 @default.
- W4229058663 cites W2987198483 @default.
- W4229058663 cites W3000522739 @default.
- W4229058663 cites W3023011061 @default.
- W4229058663 cites W3025274120 @default.
- W4229058663 cites W3031867096 @default.
- W4229058663 cites W3034951818 @default.
- W4229058663 cites W3038044033 @default.
- W4229058663 cites W3087167561 @default.
- W4229058663 cites W3107412563 @default.
- W4229058663 cites W3108559529 @default.
- W4229058663 cites W3124705062 @default.
- W4229058663 cites W3126154755 @default.
- W4229058663 cites W3154351093 @default.
- W4229058663 cites W3157511827 @default.
- W4229058663 cites W3165520006 @default.
- W4229058663 cites W3193503263 @default.
- W4229058663 cites W3206178124 @default.
- W4229058663 cites W3206542507 @default.
- W4229058663 cites W4211129961 @default.
- W4229058663 doi "https://doi.org/10.1186/s12964-022-00863-x" @default.
- W4229058663 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35513867" @default.
- W4229058663 hasPublicationYear "2022" @default.
- W4229058663 type Work @default.
- W4229058663 citedByCount "7" @default.
- W4229058663 countsByYear W42290586632022 @default.
- W4229058663 countsByYear W42290586632023 @default.
- W4229058663 crossrefType "journal-article" @default.
- W4229058663 hasAuthorship W4229058663A5000437761 @default.
- W4229058663 hasAuthorship W4229058663A5008950728 @default.
- W4229058663 hasAuthorship W4229058663A5009656164 @default.
- W4229058663 hasAuthorship W4229058663A5031340408 @default.
- W4229058663 hasAuthorship W4229058663A5035053042 @default.
- W4229058663 hasAuthorship W4229058663A5047281271 @default.
- W4229058663 hasAuthorship W4229058663A5051450048 @default.
- W4229058663 hasAuthorship W4229058663A5065437335 @default.
- W4229058663 hasAuthorship W4229058663A5085832818 @default.
- W4229058663 hasBestOaLocation W42290586631 @default.
- W4229058663 hasConcept C104317684 @default.
- W4229058663 hasConcept C127561419 @default.
- W4229058663 hasConcept C145059251 @default.
- W4229058663 hasConcept C185592680 @default.
- W4229058663 hasConcept C190283241 @default.
- W4229058663 hasConcept C203014093 @default.
- W4229058663 hasConcept C203522944 @default.