Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 291, Issue 1-2, Pages 116-124Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2008.05.005
Keywords
porcine AMSCs; Wnt/beta-catenin pathway; adipogenesis; differentiation
Categories
Funding
- The National High Technology Research and Development Program of China [2006AA10Z138]
- Major State Basic Research Development Program of China [2004CB117506]
Ask authors/readers for more resources
Wnt/beta-catenin signaling pathway controls differentiation of various cells by regulating the expression of target genes. beta-Catenin plays a central role in Wnt/beta-catenin signaling pathway. To investigate the molecular mechanisms of fate determination in adipose-derived mesenchymal stem cells (AMSCs), we investigated effects of Wnt3a and beta-catenin, two key members of the Wnt/beta-catenin signaling, in adipogenic differentiation of porcine AMSCs. We demonstrated that Wnt3a protein can inhibit the adipogenic differentiation of porcine AMSCs in vitro culture. By stabilization of cytoplasmic beta-catenin with continuous treatment by LiCl, the adipogenic differentiation of AMSCs was also suppressed and the osteogenesis was stimulated. In contrast, a loss of beta-catenin in AMSCs enhanced the adipogenic differentiation and rescued LiCl-induced anti-adipogenesis. In addition, the mutual activation of CCAAT/enhancer-binding protein-alpha (C/EBP alpha) and peroxisome proliferator-activated receptor-gamma (PPAR gamma) were repressed in the presence of Wnt3a or LiCl, but increased in the gene silencing of beta-catenin. Taken together, our study indicated that Wnt/beta-catenin signaling pathway inhibited the adipogenic differentiation potential and alter the cell fate from adipocytes to osteoblasts. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available