Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Mouse Sirt6-/- tissues

ABSTRACT: We harvested liver, spleen, thymus, and skin tissues from 21 or 29 day old Sirt6-/- animals and then completed genome-wide microarray analysis. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Amino Allyl MessageAmp II Amplification kit. Amplified age-matched wild-type tissues were used as reference RNA for analysis. Array hybridization of mouse MEEBO arrays is as described (Hendrickson et al., PLoS ONE, 2008). Set of arrays that are part of repeated experiments Tissue type: Age & tissue harvested Keywords: Biological Replicate Biological Replicate Computed

ORGANISM(S): Mus musculus

SUBMITTER: Tiara Kawahara

PROVIDER: E-GEOD-13208 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

SIRT6 links histone H3 lysine 9 deacetylation to NF-kappaB-dependent gene expression and organismal life span.

Kawahara Tiara L A TL Michishita Eriko E Adler Adam S AS Damian Mara M Berber Elisabeth E Lin Meihong M McCord Ron A RA Ongaigui Kristine C L KC Boxer Lisa D LD Chang Howard Y HY Chua Katrin F KF

Cell 20090101 1

Members of the sirtuin (SIRT) family of NAD-dependent deacetylases promote longevity in multiple organisms. Deficiency of mammalian SIRT6 leads to shortened life span and an aging-like phenotype in mice, but the underlying molecular mechanisms are unclear. Here we show that SIRT6 functions at chromatin to attenuate NF-kappaB signaling. SIRT6 interacts with the NF-kappaB RELA subunit and deacetylates histone H3 lysine 9 (H3K9) at NF-kappaB target gene promoters. In SIRT6-deficient cells, hyperace ...[more]

PMID: 19135889

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Project description:Children less than 2 years of age are capable of healing large calvarial defects, whereas adults have been found to lack this endogenous ability. In this study, we used microarray analysis to compare genomewide expression patterns during active regeneration after injury with calvaria in skeletally immature and mature mice. Parietal bone defects were created in 6-day-old (juvenile) and 60-day-old (adult) mice using a 4-mm trephine bit (n = 20 mice per age group). The calvarial disc was removed, leaving the underlying dura mater intact. Two weeks after injury, the region of regeneration with the underlying dura mater was harvested, and RNA was extracted for microarray analysis. The 25 most differentially upregulated genes in juvenile regenerates compared with adults were listed, as well as selected bone-related genes. In addition, QRT-PCR confirmation of specific genes was performed for validation. Juvenile regenerates expressed significantly greater amounts of BMP-2, -4, -7, as well as FGF-2 and its receptor FGFR-1. Various other growth factors were also noted to be upregulated, including IGF-2 and Ptn. This corresponded with the increased expression of markers for osteogenic differentiation of Sparc and Oc. Markers of osteoclast activity, Acp5, Ctsk, and Mmp2, were noted to be greater in juvenile regenerates compared with adults. The observation of Mmp14 upregulation, however, highlights the importance of balanced osteoclast-mediated bone resorption for ultimate healing. The 2 most differentially regulated genes, transthyretin (Ttr) and prostaglandin D2 synthase (Ptgds), highlight the potential role of retinoic acid signaling and the prostaglandin axis on skeletal regeneration. These findings underscore the multitude of biomolecular mechanisms at play, allowing juvenile calvaria to heal after injury. The identification of various growth factors and cytokines involved also suggests novel therapeutic strategies for tissue-engineering purposes. Set of arrays that are part of repeated experiments Elapsed Time: Calvarial regeneration in 6 day old vs 60 day old mice Biological Replicate

Dataset Information

Mouse Sirt6-/- tissues

Publications

SIRT6 links histone H3 lysine 9 deacetylation to NF-kappaB-dependent gene expression and organismal life span.

Similar Datasets

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