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Unknown,Transcriptomics,Genomics,Proteomics

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The transcription factor SOX6 contributes to the developmental origins of obesity by promoting adipogenesis through inhibition of Wnt signaling

ABSTRACT: The developmental transcription factor SOX6 was found to regulate serum, as well as liver triglycerides in BL6 mice treated with SOX6 antisense gapmers compared to control gapmers. SOX6 was initially discovered as a gene over-expressed in mesenchymal stem cells derived from small for gestational age newborns. We characterized its metabolic function in BL6 mice using the above antisense knockdown approach. BL6 mice were treated with either SOX6 specific or control gapmer oligonucleotides for 48h. Knockdown efficiency was measured in liver and epididymal white adipose tissues and serum levels of triglycerides and cholesterol quantified.

ORGANISM(S): Mus musculus

SUBMITTER: Walter Stunkel

PROVIDER: E-GEOD-70300 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The transcription factor SOX6 contributes to the developmental origins of obesity by promoting adipogenesis through inhibition of Wnt signaling

Project description:The developmental transcription factor SOX6 was found to regulate serum, as well as liver triglycerides in BL6 mice treated with SOX6 antisense gapmers compared to control gapmers. SOX6 was initially discovered as a gene over-expressed in mesenchymal stem cells derived from small for gestational age newborns. We characterized its metabolic function in BL6 mice using the above antisense knockdown approach.

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Project description:Development of LNA gapmers, antisense oligonucleotides used for efficient inhibition of target RNA expression, is limited by non-target mediated hepatotoxicity issues. In the present study, we investigated hepatic transcription profiles of mice receiving non-toxic and toxic LNA gapmers after a single and repeat administration. To understand the mechanism of LNA gapmer-induced heptotoxicity in mice, we investigated the transcription profiles of liver RNA isolated from mice receiving non-toxic sequence (NTS-1), toxic sequence (TS-2), or severely toxic sequence (HTS-3) of LNA gapmers at 25 mg/kg (dose volume of 10 mL/kg) at 8, 16, or 72 hrs after a single administration (by subcutaneous injection ) using microarray analysis. We also investigated the transcription profiles of liver RNA isolated from mice receiving non-toxic sequence (NTS-1) or toxic sequence (TS-2) of LNA gapmers at 25 mg/kg (dose volume of 10 mL/kg) at 2 weeks after repeated administration (by subcutaneous injection ) using microarray analysis.

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Project description:KDM7A Divergent Transcript (KDM7A-DT) is a stress-induced lncRNAs. In our previous studies, KDM7A-DT showed the most robust cellular phenotype alteration and a significant TP53-dependency upon oxidative and oncogenic stress induction. Since about 50% of human breast cancers have mutant p53 and associated genetic alterations, it is essential to determine what effect a mutant p53 would have on acquired pro-oncogenic functions of KDM7A-DT. In these experiments, we used four antisense LNA Gapmer sequences designed by Exiqon (Vedbaek, Denmark). One of these was a negative control, while the other 3 were designed to target the end of the transcript representing the full-length lncRNA KDM7A-DT (lncRNA; GRCh38/hg38, chr7: 140,178,951-140,179,640). To test the effect of KDM7-DT in the context of mutant p53, we selected the p53-negative luminal BC cells T47D. For each of the LNA gapmers, we utilized 3 technical replicates across two main experimental conditions (normal vs. oxidative stress induced via 30 mins of 0.2 mM H2O2 treatment). Overall, we measured the signals for 47,323 Illumina array probes across 24 individual experiments (4 LNA gapmers * 3 technical replicates * 2 main experimental conditions).

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