Abstract
Metabolic stress causes an increased Fas-FasL (receptor-ligand pair) expression in Neural Stem Cells (NSCs) leading to Fas-induced apoptosis. In this study, we discuss the exposure of NSCs to different metabolic treatments that provoke cellular stress responses. We demonstrate that challenging cultured NSCs to ethanol (ETOH) increased cellular death via Fas-mediated apoptosis. Moreover, we establish that NSCs cultured under low lipid conditions, in which they were deprived of essential fatty acids, demonstrated increased cellular survival rates suggesting an increased ability for these lipid-starved cells to endure a stressed environment. This was further confirmed by exposing NSCs to low glucose levels and observing a decrease in percent death in low lipid NSCs. When stressed, NSCs have increased reactive oxygen levels and are susceptible to apoptosis. These findings indicate that under starved and stressed conditions, and in the presence of Fas Ligand (FasL), NSCs pursue fatty acid oxidation by burning fat as fuel. This may be the key to better understand the metabolic states of brain tumors and the characteristics of cancer.
Highlights
The growing research interest in Neural Stem Cells (NSCs) is driven by the possible application of these multipotent cells as a therapeutic tool in neurodegene-rative disorders
We establish that NSCs cultured under low lipid conditions, in which they were deprived of essential fatty acids, demonstrated increased cellular survival rates suggesting an increased ability for these lipid-starved cells to endure a stressed environment
Average percent death increases by about 14% when examining low lipid (LL) compared to Normal NSCs for all treatments
Summary
The growing research interest in Neural Stem Cells (NSCs) is driven by the possible application of these multipotent cells as a therapeutic tool in neurodegene-rative disorders. Exposure to ethanol and low levels of glucose lead to limited NSC production [5,6,7,8]. They readily undergo apoptosis when environmental conditions are not ideal [9], such as altered metabolic states, hypoglycemic conditions, and ethanol-induced lipid-deprived environments [10,11,12,13,14]. Though a considerable amount of research has focused on the generation and development of neurons, the study of NSC health, growth and apoptosis in metabolic states which mimic disease states, is limited [15,16,17,18]
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