dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorBaez-Jurado, Eliana
dc.creatorVega, Gina Guio
dc.creatorAliev, Gjumrakch
dc.creatorTarasov, Vadim V.
dc.creatorEsquinas, Paula
dc.creatorEcheverria, Valentina
dc.creatorBarreto, George E.
dc.date.accessioned2023-05-24T04:21:34Z
dc.date.available2023-05-24T04:21:34Z
dc.date.created2023-05-24T04:21:34Z
dc.date.issued2018-03-01
dc.identifier0893-7648
dc.identifierhttps://repositorio.uss.cl/handle/uss/3808
dc.identifier10.1007/s12035-017-0481-y
dc.description.abstractPrevious studies have indicated that paracrine factors (conditioned medium) increase wound closure and reduce reactive oxygen species in a traumatic brain injury in vitro model. Although the beneficial effects of conditioned medium from human adipose tissue-derived mesenchymal stem cells (hMSCA-CM) have been previously suggested for various neurological diseases, their actions on astrocytic cells are not well understood. In this study, we have explored the effect of hMSCA-CM on human astrocyte model (T98G cells) subjected to scratch assay. Our results indicated that hMSCA-CM improved cell viability, reduced nuclear fragmentation, attenuated the production of reactive oxygen species, and preserved mitochondrial membrane potential and ultrastructural parameters. In addition, hMSCA-CM upregulated neuroglobin in T98G cells and the genetic silencing of this protein prevented the protective action of hMSCA-CM on damaged cells, suggesting that neuroglobin is mediating, at least in part, the protective effect of hMSCA-CM. Overall, this evidence suggests that the use of hMSCA-CM is a promising therapeutic strategy for the protection of astrocytic cells in central nervous system (CNS) pathologies.
dc.languageeng
dc.relationMolecular Neurobiology
dc.titleBlockade of Neuroglobin Reduces Protection of Conditioned Medium from Human Mesenchymal Stem Cells in Human Astrocyte Model (T98G) Under a Scratch Assay
dc.typeArtículo


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