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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Importance of histone demethylation in adipogenic differentiation and function

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE18598: Differentiating 3T3-L1 adipocytes, introduced with siRNA against aof2 and rfk genes, or treated with tranylcypromine GSE18599: Differentiating 3T3-L1 adipocytes, introduced with siRNA against phf21a gene Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Mitsuyoshi Nakao

PROVIDER: E-GEOD-18600 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure.

Hino Shinjiro S Sakamoto Akihisa A Nagaoka Katsuya K Anan Kotaro K Wang Yuqing Y Mimasu Shinya S Umehara Takashi T Yokoyama Shigeyuki S Kosai Ken-Ichiro K Nakao Mitsuyoshi M

Nature communications 20120327

Environmental factors such as nutritional state may act on the epigenome that consequently contributes to the metabolic adaptation of cells and the organisms. The lysine-specific demethylase-1 (LSD1) is a unique nuclear protein that utilizes flavin adenosine dinucleotide (FAD) as a cofactor. Here we show that LSD1 epigenetically regulates energy-expenditure genes in adipocytes depending on the cellular FAD availability. We find that the loss of LSD1 function, either by short interfering RNA or b ...[more]

PMID: 22453831

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Project description:Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. LSD1 (KDM1) protein, encoded by aof2 gene, is a histone demethylase, which is involved in transcriptional regulation. Since the enzymatic activity of LSD1 is FAD (flavin adenine dinucleotide)-dependent, its effects on gene expression may be influenced by FAD availability. To address the importance of histone demethylation in adipogenic differentiation and function, we performed cDNA microarray in LSD1-deficient 3T3-L1 cells as well as in the cells treated with LSD1 inhibitor tranylcypromine (TC). FAD-synthesizing enyme, riboflavin kinase (RFK) -deficient cells were also subjected to the microarray analysis. 3T3-L1 preadipocytes were transfected with aof2- or rfk- specific siRNA or control siRNA (siGL3) . 24 hours later, cells were subjected to adipogenic induction. 24 hours later, cells were harvested for total RNA extraction. For the TC treatment, TC was added to the adipogenic induction medium.

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