scholarly journals Chlorogenic Acids Inhibit Adipogenesis: Implications of Wnt/β-Catenin Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Mengting Liu ◽  
Jian Qin ◽  
Jing Cong ◽  
Yubin Yang
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Fatty Acid Synthase ◽  
Adipocyte Differentiation ◽  
Glycogen Synthase ◽  
Dependent Manner ◽  
Canonical Wnt Signaling ◽  
Ppar Γ ◽  
Gsk 3Β ◽  
Canonical Wnt

In our previous in vitro study, we found that chlorogenic acid (CGA) inhibited adipocyte differentiation and triglyceride (TG) accumulation, but the underlying mechanism is still unclear. Accumulative genetic evidence supports that canonical Wnt signaling is a key modulator on adipogenesis. Methods. In this study, 3T3-L1 cells were induced adipogenic differentiation and then treated with CGA. We investigate the effect of CGA in inhibiting adipogenesis and evaluate its role in modulating Wnt10b (wingless integration1 10b), β-catenin, glycogen synthase kinase-3β (GSK-3β), and peroxisome proliferator-activated receptor γ (PPAR-γ) involved in the Wnt (wingless integration1)/β-catenin signaling pathway. Results. The result showed that after CGA treatment, lipid accumulation and TG level decreased significantly in 3T3-L1 cells, indicating that CGA could inhibit adipogenesis. In addition, CGA repressed the induction of adipocyte differentiation biomarkers as PPAR-γ, adipocyte protein 2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL), and the secretion of GSK-3β in a dose-dependent manner upregulated the expression of β-catenin and Wnt10b both in gene and protein levels. Moreover, CGA induced phosphorylation of GSK-3β and promoted the accumulation of free cytosolic β-catenin in 3T3-L1 adipocytes. Conclusion. Overall, these findings gave us the implications that CGA inhibits adipogenesis via the canonical Wnt signaling pathway.

scholarly journals A divergent canonical WNT-signaling pathway regulates microtubule dynamics

2004 ◽  
Vol 164 (2) ◽  
pp. 243-253 ◽  
Author(s):  
Lorenza Ciani ◽  
Olga Krylova ◽  
Matthew J. Smalley ◽  
Trevor C. Dale ◽  
Patricia C. Salinas
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Transcriptional Activation ◽  
Glycogen Synthase ◽  
Wnt Signaling Pathway ◽  
Negative Regulator ◽  
Canonical Wnt Signaling ◽  
Microtubule Stability ◽  
Gsk 3Β ◽  
Canonical Wnt

Dishevelled (DVL) is associated with axonal microtubules and regulates microtubule stability through the inhibition of the serine/threonine kinase, glycogen synthase kinase 3β (GSK-3β). In the canonical WNT pathway, the negative regulator Axin forms a complex with β-catenin and GSK-3β, resulting in β-catenin degradation. Inhibition of GSK-3β by DVL increases β-catenin stability and TCF transcriptional activation. Here, we show that Axin associates with microtubules and unexpectedly stabilizes microtubules through DVL. In turn, DVL stabilizes microtubules by inhibiting GSK-3β through a transcription- and β-catenin–independent pathway. More importantly, axonal microtubules are stabilized after DVL localizes to axons. Increased microtubule stability is correlated with a decrease in GSK-3β–mediated phosphorylation of MAP-1B. We propose a model in which Axin, through DVL, stabilizes microtubules by inhibiting a pool of GSK-3β, resulting in local changes in the phosphorylation of cellular targets. Our data indicate a bifurcation in the so-called canonical WNT-signaling pathway to regulate microtubule stability.

The canonical Wnt signaling pathway promotes chondrocyte differentiation in a Sox9-dependent manner

2005 ◽  
Vol 333 (4) ◽  
pp. 1300-1308 ◽  
Author(s):  
Fumiko Yano ◽  
Fumitaka Kugimiya ◽  
Shinsuke Ohba ◽  
Toshiyuki Ikeda ◽  
Hirotaka Chikuda ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Chondrocyte Differentiation ◽  
Dependent Manner ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

AB0070 Wnt and wisp1 expression in the synovium induces cartilage damage by skewing of tgf-beta signaling via the canonical wnt signaling pathway

2013 ◽  
Vol 72 (Suppl 3) ◽  
pp. A807.1-A807
Author(s):  
M. H. van den Bosch ◽  
A. B. Blom ◽  
P. L. van Lent ◽  
H. M. van Beuningen ◽  
F. A. van de Loo ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Cartilage Damage ◽  
Wnt Signaling Pathway ◽  
Tgf Beta ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

scholarly journals KCTD1 Suppresses Canonical Wnt Signaling Pathway by Enhancing β-catenin Degradation

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e94343 ◽  
Author(s):  
Xinxin Li ◽  
Cheng Chen ◽  
Fangmei Wang ◽  
Wenhuan Huang ◽  
Zhongheng Liang ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

Abstract 070: Canonical Wnt Signaling Mediates Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility in Diabetic Mice

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
En Yin Lai ◽  
Suping Zhang ◽  
Qian Huang ◽  
Qiaoling Wang ◽  
Liang Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wnt Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Canonical Wnt Signaling ◽  
Protein Expressions ◽  
Afferent Arterioles ◽  
Gsk 3Β ◽  
Canonical Wnt

Background: Canonical Wnt signaling is involved in oxidative stress and diabetes but its role in diabetic renal microvascular dysfunction is unclear. We tested the hypothesis that enhanced canonical Wnt signaling in renal afferent arterioles from diabetic mice increases reactive oxygen species (ROS) and contractions to endothelin-1 (ET-1). Methods: Diabetic or control C57Bl/6 mice received vehicle or sulindac (40 mg·kg -1 ·day -1 ) to block canonical Wnt signaling for 4 weeks. ET-1 contractions were measured in diameter changes and H 2 O 2 and O 2 .- by fluorescence microscopy. Arteriolar protein expression and enzymatic activity were examined by standard methods. Results: Compared to control, diabetic mouse afferent arteriole had significantly increased O 2 .- (+84%) and H 2 O 2 (+91%) and enhanced sensitivity to ET-1 at 10 -8 mol·l -1 (-72±4% versus -43±4%, P<0.05) accompanied by significantly (P<0.005) reduced protein expressions and activities for catalase and superoxide dismutase 2 (SOD2). Incubation of afferent arterioles from normal or diabetic mice with PEG-SOD reduced responses to ET-1 whereas incubation with PEG-catalase reduced sensitivity to ET-1 selectively in arterioles from diabetic mice. The arteriolar protein expressions for canonical Wnt signaling indicated overactivation of this pathway in diabetic mice (2.6-fold increase in p-GSK-3β/GSK-3β and 3.3-fold decrease in p-β-catenin/β-catenin). Sulindac given to diabetic mice normalized the canonical Wnt signaling protein and arteriolar O 2 .- , H 2 O 2 and ET-1 contractions while doubling (P<0.05) microvascular catalase and SOD2. Conclusions: Increased ROS, notably H 2 O 2 , mediated by canonical Wnt signaling contributes to enhanced afferent arteriolar sensitivity to ET-1 in diabetes. Thus, antioxidant pharmacological strategies targeting canonical Wnt signaling may improve vascular function in diabetic nephropathy.

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