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Tibolone protects astrocytic cells from glucose deprivation through a mechanism involving estrogen receptor beta and the upregulation of neuroglobin expression
dc.contributor.author | Avila-Rodriguez M. | |
dc.contributor.author | Garcia-Segura L.M. | |
dc.contributor.author | Hidalgo-lanussa O. | |
dc.contributor.author | Baez E. | |
dc.contributor.author | Gonzalez J. | |
dc.contributor.author | Barreto G.E. | |
dc.date.accessioned | 2020-09-02T22:12:33Z | |
dc.date.available | 2020-09-02T22:12:33Z | |
dc.date.issued | 2016 | |
dc.identifier | 10.1016/j.mce.2016.05.024 | |
dc.identifier.citation | 433, , 35-46 | |
dc.identifier.issn | 03037207 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/3650 | |
dc.description | Tibolone, a synthetic steroid used for the prevention of osteoporosis and the treatment of climacteric symptoms in post-menopausal women, may exert tissue selective estrogenic actions acting on estrogen receptors (ERs). We previously showed that tibolone protects human T98G astroglial cells against glucose deprivation (GD). In this study we have explored whether the protective effect of tibolone on these cells is mediated by ERs. Experimental studies showed that both ERα and ERβ were involved in the protection by tibolone on GD cells, being ERβ preferentially involved on these actions over ERα. Tibolone increased viability of GD cells by a mechanism fully blocked by an ERβ antagonist and partially blocked by an ERα antagonist. Furthermore, ERβ inhibition prevented the effect of tibolone on nuclear fragmentation, ROS and mitochondrial membrane potential in GD cells. The protective effect of tibolone was mediated by neuroglobin. Tibolone upregulated neuroglobin in T98G cells and primary mouse astrocytes by a mechanism involving ERβ and neuroglobin silencing prevented the protective action of tibolone on GD cells. In summary, tibolone protects T98G cells by a mechanism involving ERβ and the upregulation of neuroglobin. © 2016 Elsevier Ireland Ltd. | |
dc.language.iso | en | |
dc.publisher | Elsevier Ireland Ltd | |
dc.subject | Astrocytes | |
dc.subject | ERβ | |
dc.subject | Glucose deprivation | |
dc.subject | Mitochondria | |
dc.subject | Neuroglobin | |
dc.subject | Tibolone | |
dc.subject | estrogen receptor alpha | |
dc.subject | estrogen receptor beta | |
dc.subject | glucose | |
dc.subject | messenger RNA | |
dc.subject | neuroglobin | |
dc.subject | tibolone | |
dc.subject | estrogen | |
dc.subject | estrogen receptor alpha | |
dc.subject | estrogen receptor beta | |
dc.subject | globin | |
dc.subject | nerve protein | |
dc.subject | neuroglobin | |
dc.subject | pregnane derivative | |
dc.subject | protective agent | |
dc.subject | reactive oxygen metabolite | |
dc.subject | selective estrogen receptor modulator | |
dc.subject | tibolone | |
dc.subject | animal cell | |
dc.subject | Article | |
dc.subject | astrocyte | |
dc.subject | cell protection | |
dc.subject | cell viability | |
dc.subject | controlled study | |
dc.subject | drug mechanism | |
dc.subject | gene silencing | |
dc.subject | in vitro study | |
dc.subject | male | |
dc.subject | mitochondrial membrane potential | |
dc.subject | mouse | |
dc.subject | Ngb1 gene | |
dc.subject | nonhuman | |
dc.subject | priority journal | |
dc.subject | protein expression | |
dc.subject | upregulation | |
dc.subject | animal | |
dc.subject | astrocyte | |
dc.subject | drug effects | |
dc.subject | human | |
dc.subject | metabolism | |
dc.subject | tumor cell line | |
dc.subject | Animals | |
dc.subject | Astrocytes | |
dc.subject | Cell Line, Tumor | |
dc.subject | Estrogen Receptor alpha | |
dc.subject | Estrogen Receptor beta | |
dc.subject | Estrogen Receptor Modulators | |
dc.subject | Estrogens | |
dc.subject | Globins | |
dc.subject | Glucose | |
dc.subject | Humans | |
dc.subject | Membrane Potential, Mitochondrial | |
dc.subject | Mice | |
dc.subject | Nerve Tissue Proteins | |
dc.subject | Norpregnenes | |
dc.subject | Protective Agents | |
dc.subject | Reactive Oxygen Species | |
dc.subject | Up-Regulation | |
dc.title | Tibolone protects astrocytic cells from glucose deprivation through a mechanism involving estrogen receptor beta and the upregulation of neuroglobin expression | |
dc.type | Article |