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A CREB-Sirt1-Hes1 Circuitry Mediates Neural Stem Cell Response to Glucose Availability.

Authors
  • Fusco, Salvatore1
  • Leone, Lucia2
  • Barbati, Saviana Antonella2
  • Samengo, Daniela3
  • Piacentini, Roberto2
  • Maulucci, Giuseppe4
  • Toietta, Gabriele5
  • Spinelli, Matteo2
  • McBurney, Michael6
  • Pani, Giovambattista7
  • Grassi, Claudio1
  • 1 Institute of Human Physiology, Università Cattolica Medical School, 00168 Rome, Italy; San Raffaele Pisana Scientific Institute for Research, Hospitalization and Health Care, 00163 Rome, Italy. , (Italy)
  • 2 Institute of Human Physiology, Università Cattolica Medical School, 00168 Rome, Italy. , (Italy)
  • 3 Institute of General Pathology, Università Cattolica Medical School, 00168 Rome, Italy. , (Italy)
  • 4 Institute of Physics, Università Cattolica Medical School, 00168 Rome, Italy. , (Italy)
  • 5 Regina Elena National Cancer Institute, 00144 Rome, Italy. , (Italy)
  • 6 Centre for Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, ON 81H KL6, Canada. , (Canada)
  • 7 Institute of General Pathology, Università Cattolica Medical School, 00168 Rome, Italy. Electronic address: [email protected] , (Italy)
Type
Published Article
Journal
Cell Reports
Publisher
Elsevier
Publication Date
Feb 09, 2016
Volume
14
Issue
5
Pages
1195–1205
Identifiers
DOI: 10.1016/j.celrep.2015.12.092
PMID: 26804914
Source
Medline
Keywords
License
Unknown

Abstract

Adult neurogenesis plays increasingly recognized roles in brain homeostasis and repair and is profoundly affected by energy balance and nutrients. We found that the expression of Hes-1 (hairy and enhancer of split 1) is modulated in neural stem and progenitor cells (NSCs) by extracellular glucose through the coordinated action of CREB (cyclic AMP responsive element binding protein) and Sirt-1 (Sirtuin 1), two cellular nutrient sensors. Excess glucose reduced CREB-activated Hes-1 expression and results in impaired cell proliferation. CREB-deficient NSCs expanded poorly in vitro and did not respond to glucose availability. Elevated glucose also promoted Sirt-1-dependent repression of the Hes-1 promoter. Conversely, in low glucose, CREB replaced Sirt-1 on the chromatin associated with the Hes-1 promoter enhancing Hes-1 expression and cell proliferation. Thus, the glucose-regulated antagonism between CREB and Sirt-1 for Hes-1 transcription participates in the metabolic regulation of neurogenesis.

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. This record was last updated on 07/07/2017 and may not reflect the most current and accurate biomedical/scientific data available from NLM. The corresponding record at NLM can be accessed at https://www.ncbi.nlm.nih.gov/pubmed/26804914
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