NDLI: The Wnt antagonist Dickkopf-1 and its receptors are coordinately regulated during early human adipogenesis

Content Provider	PubMed Central
Author	Christodoulides, Constantinos Matthias, Laudes Cawthorn, Will P. Schinner, Sven Soos, Maria Stephen, O’rahilly Sethi, Jaswinder K. Antonio, Vidal-puig
Abstract	Secretion of Wnts by adipose cells has an important role in the control of murine adipogenesis. We present the first evidence that a Wnt antagonist, Dickkopf 1 (Dkk1), is secreted by human preadipocytes and promotes adipogenesis. DKK1 mRNA increases six hours after onset of human adipogenesis and this is followed by an increase in Dkk1 protein. With further differentiation, the mRNA and protein levels progressively decline such that they are undetectable in mature adipocytes. The transient induction in DKK1 correlates with downregulation of cytoplasmic and nuclear β-catenin levels, this being a surrogate marker of canonical Wnt signalling, and Wnt/β-catenin transcriptional activity. In addition, constitutive expression of Dkk1 in 3T3-L1 preadipocytes promotes their differentiation, further supporting the functional significance of increased Dkk1 levels during human adipogenesis. Concomitant downregulation of the Dkk1 receptors LRP5 and LRP6 is likely to potentiate the ability of Dkk1 to inhibit Wnt signalling and promote differentiation. Notably, Dkk1 is not expressed in primary murine preadipocytes or cell lines. The involvement of Dkk1 in human but not murine adipogenesis indicates that inter-species differences exist in the molecular control of this process. Given the public health importance of disorders of adipose mass, further knowledge of the pathways involved specifically in human adipocyte differentiation might ultimately be of clinical relevance.
Related Links	http://dx.doi.org/10.1242/jcs.02975
Ending Page	2620
Page Count	8
Starting Page	2613
File Format	PDF
ISSN	00219533
e-ISSN	14779137
Journal	Journal of cell science
Issue Number	0 12
Volume Number	119
Language	English
Publisher Date	2006-06-15
Access Restriction	Open
Subject Keyword	Cell Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology

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