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Expression data from adult NSCs/neural progenitors with and without active SIRT1

ABSTRACT: We used microarrays to assess gene expression differences between proliferating adult NSCs/neural progenitors with and without active SIRT1.

ORGANISM(S): Mus musculus

PROVIDER: GSE36997 | GEO | 2015/04/01

SECONDARY ACCESSION(S): PRJNA157519

REPOSITORIES: GEO

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Expression data from adult NSCs/neural progenitors with and without active SIRT1

Project description:We used microarrays to assess gene expression differences between proliferating adult NSCs/neural progenitors with and without active SIRT1. Adult NSCs/neural progenitors were isolated from 8 week old Sirt1lox/lox and NestinCre;Sirt1lox/lox mice (129SV strain), cultured for one passage in growth factors (EGF and bFGF) before isolation at early passage 2 for RNA extraction and hybridization on Affymetrix microarrays. Gene expression data were adjusted for background and normalized using RMA.

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Phosphorylation level of SIRT1 in proliferating and senescent IMR90 cells

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The NAD+-Dependent SIRT1 Deacetylase Translates a Metabolic Switch into Regulatory Epigenetics in Skeletal Muscle Stem Cells

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Project description:Sirtuin 1 (Sirt1) has been reported to be a critical positive regulator of glucose-stimulated insulin secretion in pancreatic beta-cells. The effects on islet cells and blood glucose levels when Sirt1 is deleted specifically in the pancreas are still unclear.This study examined islet glucose responsiveness, blood glucose levels, pancreatic islet histology and gene expression in Pdx1-Cre;Sirt1(ex4F/F) mice that have loss of function and loss of expression of Sirt1 specifically in the pancreas. We found that in the Pdx1-Cre;Sirt1(ex4F/F) mice, the relative insulin positive area and the islet size distribution were unchanged. However, beta-cells were functionally impaired, presenting with lower glucose-stimulated insulin secretion. This defect was not due to a reduced expression of insulin but was associated with a decreased expression of the glucose transporter Slc2A2/Glut2 and of the Glucagon like peptide-1 receptor (Glp1r) as well as with a marked down regulation of endoplasmic reticulum (ER) chaperones that participate in the Unfolded Protein Response (UPR) pathway. Counter intuitively, the Sirt1-deficient mice did not develop hyperglycemia. Pancreatic polypeptide (PP) cells were the only other islet cells affected, with reduced numbers in the Sirt1-deficient pancreas. This study provides new mechanistic insights showing that beta-cell function in Sirt1-deficient pancreas is affected due to altered glucose sensing and deregulation of the UPR pathway. Interestingly, we uncover a context in which impaired beta-cell function is not accompanied by increased glycemia. This points to a unique compensatory mechanism. Given the reduction in PP, investigation of its role in the control of blood glucose is warranted. To uncover other Sirt1-regulated mechanisms, we performed a gene expression microarray analysis comparing pancreata from the 6 month old Sirt1âdeficient mice to their controls (n=3 per group).

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