miR-155 regulates differentiation of brown and beige adipocytes via a bistable circuit

Yong Chen, Franziska Siegel, Stefanie Kipschull, Bodo Haas, Holger Fröhlich, Gunter Meister and Alexander Pfeifer ()
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Yong Chen: Institute of Pharmacology and Toxicology, University of Bonn
Franziska Siegel: Institute of Pharmacology and Toxicology, University of Bonn
Stefanie Kipschull: Institute of Pharmacology and Toxicology, University of Bonn
Bodo Haas: Institute of Pharmacology and Toxicology, University of Bonn
Holger Fröhlich: Bonn-Aachen International Center for IT (B-IT) Algorithmic Bioinformatics
Gunter Meister: Lehrstuhl für Biochemie I, NWF III—Biologie und Vorklinische Medizin, Universität Regensburg
Alexander Pfeifer: Institute of Pharmacology and Toxicology, University of Bonn

Nature Communications, 2013, vol. 4, issue 1, 1-13

Abstract: Abstract Brown adipocytes are a primary site of energy expenditure and reside not only in classical brown adipose tissue but can also be found in white adipose tissue. Here we show that microRNA 155 is enriched in brown adipose tissue and is highly expressed in proliferating brown preadipocytes but declines after induction of differentiation. Interestingly, microRNA 155 and its target, the adipogenic transcription factor CCAAT/enhancer-binding protein β, form a bistable feedback loop integrating hormonal signals that regulate proliferation or differentiation. Inhibition of microRNA 155 enhances brown adipocyte differentiation and induces a brown adipocyte-like phenotype (‘browning’) in white adipocytes. Consequently, microRNA 155-deficient mice exhibit increased brown adipose tissue function and ‘browning’ of white fat tissue. In contrast, transgenic overexpression of microRNA 155 in mice causes a reduction of brown adipose tissue mass and impairment of brown adipose tissue function. These data demonstrate that the bistable loop involving microRNA 155 and CCAAT/enhancer-binding protein β regulates brown lineage commitment, thereby, controlling the development of brown and beige fat cells.

Date: 2013
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DOI: 10.1038/ncomms2742

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