Tibolone protects T98G cells from glucose deprivation

Rodriguez, Marco Ávila; Garcia-Segura, Luis Miguel; Cabezas, Ricardo; Torrente, Daniel; Capani, Francisco; González, Janneth; Barreto, George E.

doi:10.1016/j.jsbmb.2014.07.009

Cited by 54 publications

(54 citation statements)

References 45 publications

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“…Similarly, it has been shown that PDGF-BB suppresses peroxide accumulation in neurons and rescues cell viability against H 2 O 2 , possibly through PI3K and MAPK activation followed by an increase in catalase, glutathione peroxidase, and GSH content (Cheng and Mattson 1995;Iantomasi et al 1999;Zheng et al 2010). The maintenance of Dw m is also essential for cell survival and ATP production, and its depolarization has been associated with damaging processes such as PD and metabolic injuries like glucose deprivation, similar to what is observed during rotenone insult (Avila Rodriguez et al 2014;Barreto et al 2011;Greenamyre et al 2010;Perier and Vila 2012). Our findings also indicated that PDGF-BB protected the Dw m depolarization against rotenone in our astrocytic-like model.…”

Section: Discussionmentioning

confidence: 90%

“…Previous studies have reported a positive correlation between cell viability and morphology (Avila Rodriguez et al 2014;Xiong et al 2006), also indicating that augmented oxidative stress may induce important morphological changes. Next we evaluated whether PDGF-BB was able to preserve cell morphology under inflammatory oxidative stress with rotenone.…”

Section: Pdgf-bb Decreased Morphological Changes Induced By Rotenonementioning

confidence: 83%

“…Reactive oxygen species production was evaluated by fluorescence microscopy as previously described (Avila Rodriguez et al 2014). In brief, cells were seeded at a density of 25,000 cells per well into 24-wellplates in DMEM culture medium containing 10 % FBS and then were treated according to each experimental paradigm after 24 h of serum deprivation.…”

Section: Determination Of Reactive Oxygen Species (Ros)mentioning

confidence: 99%

“…Astrocytes are important sources of GSH (glutathione) and growth factors such as BDNF and GDNF, and are important for neuronal protection during neurodegenerative processes including traumatic brain injury, ischemia, and PD (Avila Rodriguez et al 2014; Barreto et al 2011;Cabezas et al 2012Cabezas et al , 2014Giffard and Ouyang 2004;Hirsch et al 2003;Torrente et al 2013). A previous study indicated that astrocytes co-cultured with neurons increase neuronal viability during rotenone damage (Cao et al 2007).…”

Section: Introductionmentioning

confidence: 99%

“…However, its potential neuroprotective effect in astrocytes, and its role in the regulation of rotenone-induced oxidative mechanisms have not been determined yet. In our experiments, we used human cell line T98G, as it has been broadly used in astrocytes research since they share many features with primary astrocytes and have been successfully used in our research group (Avila Rodriguez et al 2014;de Joannon et al 2000;Gasque et al 1996;Stein 1979;Torrente et al 2013).…”

Section: Introductionmentioning

confidence: 99%

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PDGF-BB Protects Mitochondria from Rotenone in T98G Cells

et al. 2014

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Rotenone is one of the most-studied neurotoxic substances as it induces oxidative stress processes both in cellular and animal models. Rotenone affects ATP generation, reactive oxygen species (ROS) production, and mitochondrial membrane potential in neurons and astrocyte-like cells. Previous epidemiologic studies have supported the role of neurotrophic factors such as BDNF and GDNF in neuroprotection mainly in neurons; however, only very few studies have focused on the importance of astrocytic protection in neurodegenerative models. In the present study, we assessed the neuroprotective effects of PDGF-BB against toxicity induced by rotenone in the astrocytic-like model of T98G human glioblastoma cell line. Our results demonstrated that pretreatment with PDGF-BB for 24 h increased cell viability, preserved nuclear morphology and mitochondrial membrane potential following stimulation with rotenone, and reduced ROS production nearly to control conditions. These observations were accompanied by important morphological changes induced by rotenone and that PDGF-BB was able to preserve cellular morphology under this toxic stimuli. These findings indicated that PDGF-BB protects mitochondrial functions, and may serve as a potential therapeutic strategy in rotenone-induced oxidative damage in astrocytes.

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Section: Discussionmentioning

confidence: 90%

Section: Pdgf-bb Decreased Morphological Changes Induced By Rotenonementioning

confidence: 83%

Section: Determination Of Reactive Oxygen Species (Ros)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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PDGF-BB Protects Mitochondria from Rotenone in T98G Cells

et al. 2014

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Raloxifene attenuates oxidative stress and preserves mitochondrial function in astrocytic cells upon glucose deprivation

Vesga-Jiménez

Hidalgo-Lanussa

Baez‐Jurado

et al. 2018

Journal Cellular Physiology

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Oxidative stress and mitochondrial dysfunction induced by metabolic insults are both hallmarks of various neurological disorders, whereby neuronal cells are severely affected by decreased glucose supply to the brain. Likely injured, astrocytes are important for neuronal homeostasis and therapeutic strategies should be directed towards improving astrocytic functions to improve brain's outcome. In the present study, we aimed to assess the actions of raloxifene, a selective estrogen receptor modulator in astrocytic cells under glucose deprivation. Our findings indicated that pretreatment with 1 µM raloxifene results in an increase in cell viability and attenuated nuclei fragmentation. Raloxifene's actions also rely on the reduction of oxidative stress and preservation of mitochondrial function in glucose‐deprived astrocytic cells, suggesting the possible direct effects of this compound on mitochondria. In conclusion, our results demonstrate that raloxifene's protective actions might be mediated in part by astrocytes in the setting of a metabolic insult.

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