scholarly journals Guanylyl cyclase/natriuretic peptide receptor-A signaling antagonizes the vascular endothelial growth factor-stimulated MAPKs and downstream effectors AP-1 and CREB in mouse mesangial cells

2012 ◽  
Vol 368 (1-2) ◽  
pp. 47-59 ◽  
Author(s):  
Satyabha Tripathi ◽  
Kailash N. Pandey
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Guanylyl Cyclase ◽  
Mesangial Cells ◽  
Vascular Endothelial ◽  
Natriuretic Peptide Receptor ◽  
Peptide Receptor ◽  
Downstream Effectors ◽  
Natriuretic Peptide Receptor A ◽  
Endothelial Growth Factor

scholarly journals Expression of vascular endothelial growth factor in response to high glucose in rat mesangial cells

2000 ◽  
Vol 165 (3) ◽  
pp. 617-624 ◽  
Author(s):  
NH Kim ◽  
HH Jung ◽  
DR Cha ◽  
DS Choi
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Diabetic Nephropathy ◽  
Growth Factor ◽  
High Glucose ◽  
Mesangial Cells ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Protein Levels ◽  
Calphostin C ◽  
Endothelial Growth Factor

Diabetic nephropathy associated with hyperglycemia is characterized by glomerular hyperfiltration and endothelial dysfunction. Vascular endothelial growth factor (VEGF) is known to be primarily involved in neoangiogenesis and increased endothelial permeability. The purpose of this study was to investigate VEGF expression in response to high glucose in rat cultured mesangial cells and to identify its signal pathway via protein kinase C (PKC). Rat mesangial cells were cultured with different concentrations of glucose: normal (5 mM d-glucose), medium (15 mM d-glucose) and high (30 mm d-glucose). Calphostin-C as a PKC inhibitor and phorbol myristate acetate (PMA) as a PKC downregulator were instillated into culture media to evaluate the role of PKC in mediating the glucose-induced increase in VEGF expression. High glucose increased expression of VEGF at the mRNA and protein levels, identified by semi-quantitative RT-PCR and western blotting, within 3 h and in a time- and glucose concentration-dependent manner. Calphostin-C and PMA inhibited glucose-induced increases in VEGF expression at the mRNA and protein levels. In conclusion, high glucose can directly increase VEGF expression in rat mesangial cells via a PKC-dependent mechanism. These results suggest that VEGF could be a potential mediator of glomerular hyperfiltration and proteinuria in diabetic nephropathy.

scholarly journals Vascular endothelial growth factor activates MAP kinase and enhances collagen synthesis in human mesangial cells

1999 ◽  
Vol 56 (6) ◽  
pp. 2055-2063 ◽  
Author(s):  
Tetsuro Amemiya ◽  
Hiroyuki Sasamura ◽  
Mizuo Mifune ◽  
Yudai Kitamura ◽  
Junichi Hirahashi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Map Kinase ◽  
Collagen Synthesis ◽  
Mesangial Cells ◽  
Vascular Endothelial ◽  
Human Mesangial Cells ◽  
Endothelial Growth Factor

scholarly journals Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells

1999 ◽  
Vol 338 (2) ◽  
pp. 367-374 ◽  
Author(s):  
Stefan FRANK ◽  
Birgit STALLMEYER ◽  
Heiko KÄMPFER ◽  
Christian SCHAFFNER ◽  
Josef PFEILSCHIFTER
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Mesangial Cells ◽  
Differential Regulation ◽  
Moderate Increase ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Endothelial Growth Factor

Under conditions associated with local and systemic inflammation, mesangial cells and invading immune cells are likely to be responsible for the release of large amounts of nitric oxide (NO) in the glomerulus. To further define the mechanisms of NO action in the glomerulus, we attempted to identify genes which are regulated by NO in rat glomerular mesangial cells. We identified vascular endothelial growth factor (VEGF) and its receptor fms-like tyrosine kinase (FLT-1) to be under the regulatory control of exogenously applied NO in these cells. Using S-nitroso-glutathione (GSNO) as an NO-donating agent, VEGF expression was strongly induced, whereas expression of its FLT-1 receptor simultaneously decreased. Expressional regulation of VEGF and FLT-1 mRNA was transient and occurred rapidly within 1–3 h after GSNO treatment. Expression of a second VEGF-specific receptor, fetal liver kinase-1 (FLK-1/KDR), could not be detected. The inflammatory cytokine interleukin-1β mediated a moderate increase in VEGF expression after 24 h and had no influence on FLT-1 expression. In contrast, platelet-derived growth factor–BB and basic fibroblast growth factor had no effect on VEGF expression, but strongly induced FLT-1 mRNA levels. Obviously, there is a differential regulation of VEGF and its receptor FLT-1 by NO, cytokines and growth factors in rat mesangial cells.

scholarly journals Interaction of Angiotensin II and Mechanical Stretch on Vascular Endothelial Growth Factor Production by Human Mesangial Cells

1999 ◽  
Vol 10 (4) ◽  
pp. 730-737
Author(s):  
GABRIELLA GRUDEN ◽  
STEPHEN THOMAS ◽  
DAVINA BURT ◽  
WUDIN ZHOU ◽  
GARY CHUSNEY ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Protein Secretion ◽  
Mesangial Cells ◽  
Fold Increase ◽  
Mechanical Stretch ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Vegf Protein

Abstract. The antiproteinuric effect of angiotensin-converting enzyme inhibitors underscores the importance of a hemodynamic injury and the renin-angiotensin system in the proteinuria of various glomerular diseases. Vascular endothelial growth factor (VEGF), a potent promoter of vascular permeability, is induced in mesangial cells by both mechanical stretch and TGF-β1. This study investigates the effect of TGF-β blockade, angiotensin II (AngII), and the interaction between AngII and stretch on human mesangial cell VEGF production. Exposure to AngII (1 μM) induced a significant increase in VEGF mRNA and protein levels (1.5 ± 0.1 and 1.7 ± 0.3, respectively, fold increase over control, P < 0.05). The AngII receptor (AT1) antagonist Losartan (10 μM) prevented AngII-induced, but not stretch-induced, VEGF protein secretion (AngII 1.7 ± 0.3, AngII + Losartan 1.0 ± 0.1, P < 0.05; stretch 2.4 ± 0.4, stretch + Losartan 2.6 ± 0.5). Stretch-induced VEGF production was also unaffected by the addition of an anti-TGF-β neutralizing antibody (stretch 2.85 ± 0.82 versus stretch + anti-TGF-β 2.84 ± 0.01, fold increase over control). Simultaneous exposure to both AngII and stretch for 12 h had an additive effect on VEGF production (AngII 1.6 ± 0.1, stretch 2.6 ± 0.27, AngII + stretch 3.1 ± 0.35). Conversely, preexposure to stretch magnified AngII-induced VEGF protein secretion (unstretched + AngII 1.3 ± 0.0, stretched + AngII 1.9 ± 0.1, P < 0.01) with a parallel 1.5-fold increase in AT1 receptor levels. AngII and stretch can both independently induce VEGF production; in addition, mechanical stretch upregulates the AT1 receptor, enhancing the cellular response to AngII.

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