Genistein Attenuates Advanced Glycation End Product-Induced Expression of Fibronectin and Connective Tissue Growth Factor

2012 ◽  
Vol 36 (1) ◽  
pp. 34-40 ◽  
Author(s):  
Mengli Tong ◽  
Yuhui Wang ◽  
Yongjun Wang ◽  
Hongyu Chen ◽  
Chengda Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Advanced Glycation ◽  
Induced Expression ◽  
Advanced Glycation End Product

Leptin and connective tissue growth factor in advanced glycation end-product-induced effects in NRK-49F cells

2004 ◽  
Vol 93 (5) ◽  
pp. 940-950 ◽  
Author(s):  
Chu-I Lee ◽  
Jinn-Yuh Guh ◽  
Hung-Chun Chen ◽  
Kuan-Hua Lin ◽  
Yu-Lin Yang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Advanced Glycation ◽  
Advanced Glycation End Product

scholarly journals Low-Density Lipoprotein Induced Expression of Connective Tissue Growth Factor via Transactivation of Sphingosine 1-Phosphate Receptors in Mesangial Cells

2012 ◽  
Vol 26 (5) ◽  
pp. 833-845 ◽  
Author(s):  
Hesham M. El-Shewy ◽  
Mimi Sohn ◽  
Parker Wilson ◽  
Mi Hye Lee ◽  
Samar M. Hammad ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Pertussis Toxin ◽  
Mesangial Cells ◽  
Tissue Growth ◽  
Low Density ◽  
Induced Expression ◽  
Sphingosine 1 Phosphate ◽  
S1p Receptor

Abstract The pro-fibrotic connective tissue growth factor (CTGF) has been linked to the development and progression of diabetic vascular and renal disease. We recently reported that low-density lipoproteins (LDL) induced expression of CTGF in aortic endothelial cells. However, the molecular mechanisms are not fully defined. Here, we have studied the mechanism by which LDL regulates CTGF expression in renal mesangial cells. In these cells, treatment with pertussis toxin abolished LDL-stimulated activation of ERK1/2 and c-Jun N-terminal kinase (JNK), indicating the involvement of heterotrimeric G proteins in LDL signaling. Treatment with LDL promoted activation and translocation of endogenous sphingosine kinase 1 (SK1) from the cytosol to the plasma membrane concomitant with production of sphingosine-1-phosphate (S1P). Pretreating cells with SK inhibitor, dimethylsphinogsine or down-regulation of SK1 and SK2 revealed that LDL-dependent activation of ERK1/2 and JNK is mediated by SK1. Using a green fluorescent protein-tagged S1P1 receptor as a biological sensor for the generation of physiologically relevant S1P levels, we found that LDL induced S1P receptor activation. Pretreating cells with S1P1/S1P3 receptor antagonist VPC23019 significantly inhibited activation of ERK1/2 and JNK by LDL, suggesting that LDL elicits G protein-dependent activation of ERK1/2 and JNK by stimulating SK1-dependent transactivation of S1P receptors. Furthermore, S1P stimulation induced expression of CTGF in a dose-dependent manner that was markedly inhibited by blocking the ERK1/2 and JNK signaling pathways. LDL-induced CTGF expression was pertussis toxin sensitive and inhibited by dimethylsphinogsine down-regulation of SK1 and VPC23019 treatment. Our data suggest that SK1-dependent S1P receptor transactivation is upstream of ERK1/2 and JNK and that all three steps are required for LDL-regulated expression of CTGF in mesangial cells.

scholarly journals ALK-5 Mediates Endogenous and TGF-β1–Induced Expression of Connective Tissue Growth Factor in Embryonic Lung

2007 ◽  
Vol 36 (5) ◽  
pp. 552-561 ◽  
Author(s):  
Shu Wu ◽  
Jinghong Peng ◽  
Matthew R. Duncan ◽  
Kalyani Kasisomayajula ◽  
Gary Grotendorst ◽  
...  
Keyword(s):  
Growth Factor ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Embryonic Lung ◽  
Induced Expression ◽  
Alk 5 ◽  
Tgf Β1

scholarly journals Src Inhibition Attenuates Liver Fibrosis by Preventing Hepatic Stellate Cell Activation and Decreasing Connective Tissue Growth Factor

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 558 ◽  
Author(s):  
Hye-Young Seo ◽  
So-Hee Lee ◽  
Ji-Ha Lee ◽  
Yu Na Kang ◽  
Jae Seok Hwang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Fibrosis ◽  
Connective Tissue ◽  
Connective Tissue Growth Factor ◽  
Mouse Liver ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Tissue Growth ◽  
Type I ◽  
Induced Expression

The SRC kinase family comprises non-receptor tyrosine kinases that are ubiquitously expressed in all cell types. Although Src is reportedly activated in pulmonary and renal fibrosis, little is known regarding its role in liver fibrosis. This study investigated whether the inhibition of Src protects against liver fibrosis. The expression of Src was upregulated in thioacetamide (TAA)-induced fibrotic mouse liver and cirrhosis of patients, and phospho-Src was upregulated during activation of hepatic stellate cells (HSC). In addition, Src inhibition reduced the expression of α-smooth muscle actin (αSMA) in primary HSCs and suppressed transforming growth factor β (TGF-β)-induced expression of connective tissue growth factor (CTGF) in hepatocytes. Src inhibitor Saracatinib also attenuated TAA-induced expression of type I collagen, αSMA, and CTGF in mouse liver tissues. The antifibrotic effect of Src inhibitors was associated with the downregulation of Smad3, but not of signal transducer and activator of transcription 3 (STAT3). In addition, Src inhibition increased autophagy flux and protected against liver fibrosis. These results suggest that Src plays an important role in liver fibrosis and that Src inhibitors could be treat liver fibrosis.

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