ArticleJournal of molecular neuroscience : MN2016
Mitochondrial c-Fos May Increase the Vulnerability of Neuro2a Cells to Cellular Stressors.
Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- Neuroprotective Effects of Low-Dose Graphenic Materials on SN4741 Embryonic Stem Cells Against ER Stress and MPTP-Induced Oxidative Stress.International journal of molecular sciences · 2025Article
- Pituitary Adenylate Cyclase-Activating Polypeptide in the Ventromedial Hypothalamus Is Responsible for Food Intake Behavior by Modulating the Expression of Agouti-Related Peptide in Mice.Molecular neurobiology · 2020Article
- Protective Effects of Quercetin on Mitochondrial Biogenesis in Experimental Traumatic Brain Injury via the Nrf2 Signaling Pathway.PloS one · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Although c-Fos expression in mitochondria is known to increase under excitatory injury via kainic acid or N-methyl-D-aspartate injection, the authentic function of c-Fos in mitochondria remains unknown. We found that c-Fos expression in the mitochondria of neuroblastoma Neuro2a cells was augmented by oxygen and glucose deprivation (OGD), which is a common in vitro model for brain ischemia. Then we demonstrated that Neuro2a cells stably expressing c-Fos exclusively in the mitochondria were more vulnerable to stressors such as OGD, rotenone (which is known to induce mitochondrial dysfunction) and hydrogen peroxide (a reactive oxygen species). Since mitochondrial dysfunction and the generation of reactive oxygen species are known to be caused by OGD, our findings indicate that mitochondrial c-Fos increases neuronal vulnerability to brain ischemia. This suggests that mitochondrial c-Fos play a potential role in inducing neuronal death on, and can therefore act as a potential drug target for brain ischemia.
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