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- W1967156900 abstract "The low survival and differentiation rates of stem cells after either transplantation or neural injury have been a major concern of stem cell-based therapy. Thus, further understanding long-term survival and differentiation of stem cells may uncover new targets for discovery and development of novel therapeutic approaches. We have previously described the impact of mitochondrial apoptosis-related events in modulating neural stem cell (NSC) fate. In addition, the endogenous bile acid, tauroursodeoxycholic acid (TUDCA) was shown to be neuroprotective in several animal models of neurodegenerative disorders by acting as an anti-apoptotic and anti-oxidant molecule at the mitochondrial level. Here, we hypothesize that TUDCA might also play a role on NSC fate decision. We found that TUDCA prevents mitochondrial apoptotic events typical of early-stage mouse NSC differentiation, preserves mitochondrial integrity and function, while enhancing self-renewal potential and accelerating cell cycle exit of NSCs. Interestingly, TUDCA prevention of mitochondrial alterations interfered with NSC differentiation potential by favoring neuronal rather than astroglial conversion. Finally, inhibition of mitochondrial reactive oxygen species (mtROS) scavenger and adenosine triphosphate (ATP) synthase revealed that the effect of TUDCA is dependent on mtROS and ATP regulation levels. Collectively, these data underline the importance of mitochondrial stress control of NSC fate decision and support a new role for TUDCA in this process." @default.
- W1967156900 created "2016-06-24" @default.
- W1967156900 creator A5027045745 @default.
- W1967156900 creator A5051760428 @default.
- W1967156900 creator A5074043200 @default.
- W1967156900 creator A5086115754 @default.
- W1967156900 date "2014-10-29" @default.
- W1967156900 modified "2023-09-26" @default.
- W1967156900 title "Tauroursodeoxycholic acid increases neural stem cell pool and neuronal conversion by regulating mitochondria-cell cycle retrograde signaling" @default.
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- W1967156900 doi "https://doi.org/10.4161/15384101.2014.962951" @default.
- W1967156900 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4613652" @default.
- W1967156900 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25483094" @default.
- W1967156900 hasPublicationYear "2014" @default.
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