[show abstract][hide abstract] ABSTRACT: The Wnt/beta-catenin signaling pathway alters adipocyte differentiation by inhibiting adipogenic gene expression. beta-catenin plays a central role in the Wnt/beta-catenin signaling pathway. In this study, we revealed that tumour necrosis factor-alpha (TNF-alpha), a potential negative regulator of adipocyte differentiation, inhibits porcine adipogenesis through activation of the Wnt/beta-catenin signaling pathway. Under the optimal concentration of TNF-alpha, the intracellular beta-catenin protein was stabilized. Thus, the intracellular lipid accumulation of porcine preadipocyte was suppressed and the expression of important adipocyte marker genes, including peroxisome proliferator-activated receptor-gamma (PPARgamma) and CCAAT/enhancer binding protein-alpha (C/EBPalpha), were inhibited. However, a loss of beta-catenin in porcine preadipocytes enhanced the adipogenic differentiation and attenuated TNF-alpha induced anti-adipogenesis. Taken together, this study indicated that TNF-alpha inhibits adipogenesis through stabilization of beta-catenin protein in porcine preadipocytes.
[show abstract][hide abstract] ABSTRACT: 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/EBPalpha) and peroxisome proliferator-activated receptor-gamma (PPARgamma) 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.
Molecular and Cellular Endocrinology 06/2008; 291(1-2):116-24. · 4.04 Impact Factor
[show abstract][hide abstract] ABSTRACT: To investigate effects of docosahexaenoic acid (DHA) on proliferation and differentiation of rat adipocytes and to elucidate its potential mechanism, rat's primary preadipocytes in vitro were cultured. Treated adipocytes with 0 micromol/L (control group), 40 micromol/L (lower dose group) and 160 micromol/L (higher dose group) DHA. Cell living rations and proliferation were analyzed by trypan blue exclusion and MTT assay. The degree of adipogenesis and differentiation were measured by Oil Red O staining extraction assay and the expression of peroxisome proliferation activated receptor-gamma2 (PPARgamma2) mRNA were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). It was demonstrated that cells living ration and the optical density (OD) of MTT were all decreased, especially treated by 160 micromol/L DHA at 60 (72 hours (P < 0.05). The OD of Oil Red O staining and the expression of PPARgamma2 mRNA were all decreased after treated by 160 micromol/L DHA (P < 0.01). It can be concluded that DHA can inhibite proliferation and differentiation of adipocytes in some degree. Higher dose of DHA can markedly decrease adipogenesis and prevent differentiation of adipocytes, which may be in part associated with its effect on decreasing the expression of PPARgamma2 mRNA.
Sheng wu gong cheng xue bao = Chinese journal of biotechnology 09/2005; 21(5):840-3.