PMID- 21514273
OWN - NLM
STAT- MEDLINE
DCOM- 20110726
LR  - 20110516
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 408
IP  - 3
DP  - 2011 May 13
TI  - Msx2 is required for TNF-alpha-induced canonical Wnt signaling in 3T3-L1 
      preadipocytes.
PG  - 399-404
LID - 10.1016/j.bbrc.2011.04.029 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) is known to suppress adipocyte differentiation 
      via a beta-catenin-dependent pathway. However, the mechanisms by which TNF-alpha induces 
      Wnt/beta-catenin signaling pathway in adipocytes is unclear. Msx2, a homeobox 
      transcription factor, is known to increase osteoblast differentiation through 
      activation of the Wnt/beta-catenin pathway. Therefore, in the present study, we 
      investigated whether TNF-alpha activates the Wnt/beta-catenin signaling pathway via the 
      induction of Msx2 expression in 3T3-L1 preadipocytes. We found that TNF-alpha 
      transiently increased Msx2 expression as well as the expression of canonical Wnt 
      signaling molecules, including Wnt3a, Wnt7a, Wnt7b, Wnt10b, low-density 
      lipoprotein receptor-related protein 5 (LRP5) and T-cell factor 1 (TCF1). 
      Furthermore, TNF-alpha increased beta-catenin/TCF-dependent transcriptional activity. To 
      better understand the role of Msx2 in Wnt signaling, we examined the effects of 
      Msx2 overexpression and knockdown on Wnt/beta-catenin signaling. Msx2 overexpression 
      alone significantly increased the levels of Wnt3a, Wnt7a, Wnt7b, Wnt10b, LRP5 and 
      TCF1 expression, whereas knockdown of Msx2 using small interfering RNA prevented 
      TNF-alpha-induced expression of Wnt signaling molecules. Taken together, the results 
      of this study indicate that TNF-alpha enhances the Wnt/beta-catenin signaling pathway by 
      inducing Msx2 expression, which in turn suppresses adipocytic differentiation.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Qadir, Abdul S
AU  - Qadir AS
AD  - Department of Molecular Genetics, School of Dentistry and Dental Research 
      Institute, Seoul National University, Seoul 110-749, Republic of Korea.
FAU - Lee, Hye-Lim
AU  - Lee HL
FAU - Baek, Kyung Hwa
AU  - Baek KH
FAU - Park, Hyun-Jung
AU  - Park HJ
FAU - Woo, Kyung Mi
AU  - Woo KM
FAU - Ryoo, Hyun-Mo
AU  - Ryoo HM
FAU - Baek, Jeong-Hwa
AU  - Baek JH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110413
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Homeodomain Proteins)
RN  - 0 (MSX2 protein)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Wnt Proteins)
RN  - 0 (beta Catenin)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/drug effects/*metabolism
MH  - *Adipogenesis/drug effects
MH  - Animals
MH  - Gene Knockdown Techniques
MH  - Homeodomain Proteins/genetics/*metabolism
MH  - Humans
MH  - Mice
MH  - Recombinant Proteins/pharmacology
MH  - Signal Transduction/drug effects
MH  - Tumor Necrosis Factor-alpha/pharmacology/*physiology
MH  - Wnt Proteins/*metabolism
MH  - beta Catenin/*metabolism
EDAT- 2011/04/26 06:00
MHDA- 2011/07/27 06:00
CRDT- 2011/04/26 06:00
PHST- 2011/03/08 00:00 [received]
PHST- 2011/04/06 00:00 [accepted]
PHST- 2011/04/26 06:00 [entrez]
PHST- 2011/04/26 06:00 [pubmed]
PHST- 2011/07/27 06:00 [medline]
AID - S0006-291X(11)00603-6 [pii]
AID - 10.1016/j.bbrc.2011.04.029 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2011 May 13;408(3):399-404. doi: 
      10.1016/j.bbrc.2011.04.029. Epub 2011 Apr 13.