DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hou, Jingang | ko |
dc.contributor.author | Yun, Yeejin | ko |
dc.contributor.author | Xue, Jianjie | ko |
dc.contributor.author | Sun, Mengqi | ko |
dc.contributor.author | Kim, Sunchang | ko |
dc.date.accessioned | 2019-11-04T05:20:18Z | - |
dc.date.available | 2019-11-04T05:20:18Z | - |
dc.date.created | 2019-11-04 | - |
dc.date.created | 2019-11-04 | - |
dc.date.issued | 2019-11 | - |
dc.identifier.citation | MOLECULAR MEDICINE REPORTS, v.20, no.5, pp.4111 - 4118 | - |
dc.identifier.issn | 1791-2997 | - |
dc.identifier.uri | http://hdl.handle.net/10203/268190 | - |
dc.description.abstract | The 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.language | English | - |
dc.publisher | SPANDIDOS PUBL LTD | - |
dc.title | D-galactose induces astrocytic aging and contributes to astrocytoma progression and chemoresistance via cellular senescence | - |
dc.type | Article | - |
dc.identifier.wosid | 000491393100014 | - |
dc.identifier.scopusid | 2-s2.0-85073059663 | - |
dc.type.rims | ART | - |
dc.citation.volume | 20 | - |
dc.citation.issue | 5 | - |
dc.citation.beginningpage | 4111 | - |
dc.citation.endingpage | 4118 | - |
dc.citation.publicationname | MOLECULAR MEDICINE REPORTS | - |
dc.identifier.doi | 10.3892/mmr.2019.10677 | - |
dc.contributor.localauthor | Kim, Sunchang | - |
dc.contributor.nonIdAuthor | Hou, Jingang | - |
dc.contributor.nonIdAuthor | Xue, Jianjie | - |
dc.contributor.nonIdAuthor | Sun, Mengqi | - |
dc.description.isOpenAccess | Y | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | D-galactose | - |
dc.subject.keywordAuthor | astrocytic CRT cells | - |
dc.subject.keywordAuthor | senescence | - |
dc.subject.keywordAuthor | brain tumor | - |
dc.subject.keywordAuthor | chemoresistance | - |
dc.subject.keywordPlus | OXIDATIVE DAMAGE | - |
dc.subject.keywordPlus | MEMORY LOSS | - |
dc.subject.keywordPlus | BRAIN | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | INVOLVEMENT | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | CELLS | - |
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