D-galactose induces astrocytic aging and contributes to astrocytoma progression and chemoresistance via cellular senescence

Cited 20 time in webofscience Cited 10 time in scopus
  • Hit : 818
  • Download : 131
DC FieldValueLanguage
dc.contributor.authorHou, Jingangko
dc.contributor.authorYun, Yeejinko
dc.contributor.authorXue, Jianjieko
dc.contributor.authorSun, Mengqiko
dc.contributor.authorKim, Sunchangko
dc.date.accessioned2019-11-04T05:20:18Z-
dc.date.available2019-11-04T05:20:18Z-
dc.date.created2019-11-04-
dc.date.created2019-11-04-
dc.date.issued2019-11-
dc.identifier.citationMOLECULAR MEDICINE REPORTS, v.20, no.5, pp.4111 - 4118-
dc.identifier.issn1791-2997-
dc.identifier.urihttp://hdl.handle.net/10203/268190-
dc.description.abstractThe administration of D-galactose triggers brain aging by poorly understood mechanisms. It is generally recognized that D-galactose induces oxidative stress or affects protein modifications via receptors for advanced glycated end products in a variety of species. In the present study, we aimed to investigate the involvement of astrocytes in D-galactose-induced brain aging in vitro. We found that D-galactose treatment significantly suppressed cell viability and induced cellular senescence. In addition, as of the accumulation of senescent cells, we proposed that the senescence-associated secretory phenotype (SASP) can stimulate age-related pathologies and chemoresistance in brain. Consistently, senescent astrocytic CRT cells induced by D-galactose exhibited increases in the levels of IL-6 and IL-8 via NF-kappa B activation, which are major SASP components and inflammatory cytokines. Conditioned medium prepared from senescent astrocytic CRT cells significantly promoted the viability of brain tumor cells (U373-MG and N2a). Importantly, conditioned medium greatly suppressed the cytotoxicity of U373-MG cells induced by temozolomide, and reduced the protein expression levels of neuron marker neuron-specific class III beta-tubulin, but markedly increased the levels of c-Myc in N2a cells. Thus, our findings demonstrated that D-galactose treatment might mimic brain aging, and that D-galactose could contribute to brain inflammation and tumor progression through inducing the accumulation of senescent-secretory astrocytes.-
dc.languageEnglish-
dc.publisherSPANDIDOS PUBL LTD-
dc.titleD-galactose induces astrocytic aging and contributes to astrocytoma progression and chemoresistance via cellular senescence-
dc.typeArticle-
dc.identifier.wosid000491393100014-
dc.identifier.scopusid2-s2.0-85073059663-
dc.type.rimsART-
dc.citation.volume20-
dc.citation.issue5-
dc.citation.beginningpage4111-
dc.citation.endingpage4118-
dc.citation.publicationnameMOLECULAR MEDICINE REPORTS-
dc.identifier.doi10.3892/mmr.2019.10677-
dc.contributor.localauthorKim, Sunchang-
dc.contributor.nonIdAuthorHou, Jingang-
dc.contributor.nonIdAuthorXue, Jianjie-
dc.contributor.nonIdAuthorSun, Mengqi-
dc.description.isOpenAccessY-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorD-galactose-
dc.subject.keywordAuthorastrocytic CRT cells-
dc.subject.keywordAuthorsenescence-
dc.subject.keywordAuthorbrain tumor-
dc.subject.keywordAuthorchemoresistance-
dc.subject.keywordPlusOXIDATIVE DAMAGE-
dc.subject.keywordPlusMEMORY LOSS-
dc.subject.keywordPlusBRAIN-
dc.subject.keywordPlusMICE-
dc.subject.keywordPlusINVOLVEMENT-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordPlusCELLS-
This item is cited by other documents in WoS
⊙ Detail Information in WoSⓡ Click to see webofscience_button
⊙ Cited 20 items in WoS Click to see citing articles in records_button

qr_code

  • mendeley

    citeulike


rss_1.0 rss_2.0 atom_1.0