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Potential neuroprotective effects of SIRT1 induced by glucose deprivation in PC12 cells.

Authors: Fujino, K  Ogura, Y  Sato, K  Nedachi, T 
Citation: Fujino K, etal., Neurosci Lett. 2013 Dec 17;557 Pt B:148-53. doi: 10.1016/j.neulet.2013.10.050. Epub 2013 Oct 29.
Pubmed: (View Article at PubMed) PMID:24183892
DOI: Full-text: DOI:10.1016/j.neulet.2013.10.050

Nutrient availability is one of the most important signals regulating cellular fates including cell growth, differentiation, and death. Recent evidence suggests that the NAD(+)-dependent histone deacetylase sirtuin 1 (SIRT1) plays a prominent role in linking changes in nutritional availability with cellular fate regulation. SIRT1 expression is observed in neurons, yet the expressional and functional regulation of this protein is not fully understood. In the present study, we examined whether extracellular glucose concentration affects the expression and localization of SIRT1 in PC12 cells. Further, we examined levels of forkhead box O3a (FoxO3a), which is also controlled by changes in extracellular glucose concentration. We observed the total expression levels of SIRT1 and FoxO3a in PC12 cells were reduced when glucose availability increased via gene expressional control, at least in part. Nuclear localization of SIRT1 and FoxO3a was increased by glucose deprivation. Even though the changes in extracellular glucose concentration regulated SIRT1 and FoxO3a in a similar direction, the effects of nerve growth factor on these two proteins were completely different. Finally, we found the potent SIRT1 inhibitor enhanced glucose deprivation-induced cell death. Therefore, we propose that glucose deprivation-induced SIRT1 expression potentially plays a major role in protecting PC12 cells.


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CRRD Object Information
CRRD ID: 9495918
Created: 2014-09-17
Species: All species
Last Modified: 2014-09-17
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.