Small-interference RNA-mediated knock-down of aldehyde oxidase 1 in 3T3-L1 cells impairs adipogenesis and adiponectin release

Aldehyde oxidase 1 (AOX1) is highly abundant in the liver and oxidizes aldehydes thereby generating reactive oxygen species. Enzymes involved in detoxification of aldehydes are expressed in adipocytes and alter adipogenesis, therefore the functional role of AOX1 in adipocytes was analyzed. AOX1 mRNA...

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Bibliographic Details
Published in:FEBS letters 2008-08, Vol.582 (19), p.2965-2972
Main Authors: Weigert, Johanna, Neumeier, Markus, Bauer, Sabrina, Mages, Wolfgang, Schnitzbauer, Andreas A., Obed, Aiman, Gröschl, Benedikt, Hartmann, Arndt, Schäffler, Andreas, Aslanidis, Charalampos, Schölmerich, Jürgen, Buechler, Christa
Format: Article
Language:English
Subjects:
3T3-L1 Cells
Adipocytes
Adipocytes - drug effects
Adipocytes - enzymology
Adipogenesis - drug effects
Adipogenesis - genetics
Adiponectin - metabolism
Adipose tissue
Aldehyde Oxidoreductases - genetics
Aldehyde Oxidoreductases - physiology
Animals
Fenofibrate - pharmacology
Mice
Peroxisome proliferator-activated receptor agonist
RNA, Small Interfering - genetics
Thiazolidinediones - pharmacology
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Summary:Aldehyde oxidase 1 (AOX1) is highly abundant in the liver and oxidizes aldehydes thereby generating reactive oxygen species. Enzymes involved in detoxification of aldehydes are expressed in adipocytes and alter adipogenesis, therefore the functional role of AOX1 in adipocytes was analyzed. AOX1 mRNA was higher in visceral compared to subcutaneous human adipose tissue but AOX1 protein was detected in both fat depots. AOX1 expression in adipocytes was confirmed by immunohistochemistry and immunoblot. AOX1 was induced during adipocytic differentiation and was downregulated by fenofibrate in differentiated cells. Knock-down of AOX1 in preadipocytes led to impaired lipid storage and adiponectin release in the differentiated cells. These data indicate that AOX1 is essential for adipogenesis and may link energy and drug metabolism.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2008.07.034