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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse transgenics with cardiac specific overexpression of Sirt1 (Tg-Sirt1) and non-transgenic (NTg) control littermate at 3 months of age

ABSTRACT: We harvested the heart from transgenic mice with cardiac specific overexpression of Sirt1 (Tg-Sirt1) and non-transgenic (NTg) control littermate at 3 months of age and then microarray analyses were conducted. Experiment Overall Design: Two transgenic mice and two wild type mice were used.

ORGANISM(S): Mus musculus

SUBMITTER: Bin Tian

PROVIDER: E-GEOD-7407 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Sirt1 regulates aging and resistance to oxidative stress in the heart.

Alcendor Ralph R RR Gao Shumin S Zhai Peiyong P Zablocki Daniela D Holle Eric E Yu Xianzhong X Tian Bin B Wagner Thomas T Vatner Stephen F SF Sadoshima Junichi J

Circulation research 20070419 10

Silent information regulator (Sir)2, a class III histone deacetylase, mediates lifespan extension in model organisms and prevents apoptosis in mammalian cells. However, beneficial functions of Sir2 remain to be shown in mammals in vivo at the organ level, such as in the heart. We addressed this issue by using transgenic mice with heart-specific overexpression of Sirt1, a mammalian homolog of Sir2. Sirt1 was significantly upregulated (4- to 8-fold) in response to pressure overload and oxidative s ...[more]

PMID: 17446436

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Regulation of Gene Expression by Sirt1 in the heart

Project description:We harvested the heart from transgenic mice with cardiac specific overexpression of Sirt1 (Tg-Sirt1) and non-transgenic (NTg) control littermate at 3 months of age and then microarray analyses were conducted. Keywords: Gene expression comparison

2007-03-31 | GSE7407 | GEO

Gene expression profiles in Sirt1/PPARalpha bigenic mice

Project description:Cardiac-specific PPARalpha transgenic (Tg-PPARalpha) mice show mild cardiac hypertrophy and systolic dysfunction. The failing heart phenotypes observed in Tg-PPARalpha are exacerbated by crossing with cardiac-specific Sirt1 transgenic (Tg-Sirt1) mice, whereas Tg-Sirt1 mice themselves do not show any cardiac hypertrophy or systolic dysfunction. To investigate the mechanism leading to the failing heart phenotypes in TgPPARalpha/Tg-Sirt1 bigenic mice, microarray analyses were performed. The microarray analyses revealed that many ERR target genes were downregulated in Tg-PPARalpha and in Tg-Sirt1, and they were further downregulated in the Tg-PPARalpha/Tg-Sirt1 bigenic mice. Four groups of cardiac-specific transgenic mice were used for the study, i.e., control, PPARalpha, Sirt1 and PPARalpha/Sirt1. Hearts were dissected after 10-11 weeks of male FVB background transgenic mice. Total RNA was prepared from the hearts to conduct the microarray analyses.

2011-12-01 | E-GEOD-33101 | biostudies-arrayexpress

Gene expression profiles in Sirt1/PPARalpha bigenic mice

2011-12-01 | GSE33101 | GEO

Renal tubular Sirt1 attenuates diabetic albuminuria by epigenetically suppressing Claudin-1 overexpression in podocytes.

Project description:We aim to investigate the role of renal Sirt1 on albuminuria. To further development of our gene expression approach to biodosimetry, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish between wild type(C57BL/6J) mice treated with streptozotocin (WT+STZ) and Sirt1-overexpressing transgenic mice treated with streptozotocin (TG+STZ) mice. To elucidate the molecular mechanisms underlying the amelioration of albuminuria by our TG (Sirt1-overexpressing transgenic) mice, we performed DNA microarray analysis using micro-dissected glomerular regions to examine the differences in gene expression between WT+STZ and TG+STZ mice.

2018-03-08 | GSE50140 | GEO

SIRT1 regulates enhanced mitochondrial respiration and leukemogenicity in CML stem cells

Project description:Chronic myeloid leukemia (CML) results from hematopoietic stem cell transformation by the BCR-ABL tyrosine kinase. We have shown that the SIRT1 deacetylase is overexpressed in CML LSC, and may contribute to their maintenance. Here, using genetic deletion of SIRT1 in transgenic CML mice, we definitively demonstrate that SIRT1 is required for leukemia development, and reveal its critical role in mediating increased mitochondrial respiration in CML LSC.

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Sirt1 targeting promotes Treg function

Project description:Sirtuin-1 (Sirt1), a class III histone/protein deacetylase is central to cellular metabolism, stress responses and aging, but its contributions to various host immune functions have been little investigated. To study the role of Sirt1 in T-cell functions, we undertook targeted deletions by mating mice with a floxed Sirt1 gene to mice expressing CD4-cre or Foxp3-cre recombinase, respectively. We found that Sirt1 deletion left conventional T-effector cell activation, proliferation and cytokine production largely unaltered. However, Sirt1 targeting promoted the expression and acetylation of Foxp3, a key transcription factor in T-regulatory (Treg) cells, and increased Treg suppressive functions in vitro and in vivo. Consistent with these data, mice with targeted deletions of Sirt1 in either CD4+ T-cells or Foxp3+ Treg cells exhibited prolonged survival of MHC-mismatched cardiac allografts. Allografts in Sirt1 targeted recipients showed long-term preservation of myocardial histology and infiltration by Foxp3+ Treg cells. Comparable results were seen in wild-type allograft recipients treated with Sirt1 inhibitors, such as EX-527 and splitomicin. Hence, Sirt1 may inhibit Treg functions and its targeting may have therapeutic value in autoimmunity and transplantation. RNA from three independent samples from magnetically separated CD4+CD25+ Treg of Sirt1 knock out, compared to wild type (C57BL6) control

2011-01-05 | E-GEOD-26425 | biostudies-arrayexpress

Sirt1 targeting promotes Treg function

2011-01-05 | GSE26425 | GEO

Sirt1-microRNA profile

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2010-06-24 | GSE22530 | GEO

Sirt1-microRNA profile

Project description:Sirt1, a NAD-dependent deacetylase, has been shown involved in many complex biological functions. We previously demonstrated that Sirt-1 gain of function is neuroprotective in a model of neurodegenenration. We recently found that Sirt1 loss of function (Sirt1Î mouse) impairs learning, memory, and synaptic plasticity. We used microarray screening to identify potential miRNAs that may be regulated by Sirt1 and ivolved in learning and memory. Total RNA from the hippocampus of SIRT1Î and control mice was extracted and used for microRNA expression level evaluation. Two group experiment, in duplicates. Each sample is compared to a common reference sample, comprised of an equal mixture of all 4 experimental samples.

2010-07-29 | E-GEOD-22530 | biostudies-arrayexpress

Intestinal SIRT1 in the regulation of intestinal tissue homeostasis

Project description:The goal of this project is to investigate the role of SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, in the regulation of intestinal tissue integrity. Using a mouse model with specific deletion of SIRT1 in intestinal epithelium (SIRT1 iKO mice), we recently discovered that deletion of intestinal SIRT1 in mice age-dependently elicits NF-κB signaling and other stress response pathways, activates intestinal secretory cells, enhances spontaneous inflammation, and alters commensal gut microbial composition. To understand the molecular mechanisms underlying these age-dependent phenotypes, we examined the transcriptomes of young (6-8 week old) and aged (24-month old) ilea and aged colons from Flox controls and SIRT1 iKO mice by microarray analysis.

2017-05-30 | GSE86475 | GEO

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