scholarly journals Tumor necrosis factor-mediated release of platelet-derived growth factor from cultured endothelial cells.

1987 ◽  
Vol 166 (1) ◽  
pp. 235-245 ◽  
Author(s):  
K A Hajjar ◽  
D P Hajjar ◽  
R L Silverstein ◽  
R L Nachman
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Umbilical Vein ◽  
Fold Increase ◽  
Mitogenic Activity ◽  
Platelet Derived Growth Factor ◽  
Adhesive Properties ◽  
Necrosis Factor

Platelet-derived growth factor (PDGF) is a 30,000-Mr glycoprotein that is chemotactic and mitogenic for vascular smooth muscle cells (SMC). It is also a potent vasoconstrictor. In the present study, we found that the macrophage-derived polypeptide, tumor necrosis factor (TNF), releases a factor from human umbilical vein endothelial cells (EC) that is mitogenic for SMC. Postculture medium from TNF-stimulated EC induced a 90% increase in mitogenesis is compared with controls. This effect was half-maximal at a TNF dose of 114 pM, reflected a 2.5-fold increase in PDGF-specific mRNA synthesis, and peaked at 15 h of TNF stimulation. Mitogenic activity was completely abrogated by preincubation of postculture medium with antibody to platelet PDGF. Stimulation of EC with IL-1 (60-240 pM) led to the release of similar mitogenic activity. Thus, in addition to its effects on the hemostatic and adhesive properties of EC, TNF also promotes release of PDGF, which may serve to modulate proliferation of vascular SMC during wound healing, inflammation, and atherogenesis.

scholarly journals Interleukin-1, tumor necrosis factor, and the production of colony- stimulating factors by cultured mesenchymal cells

Blood ◽  
1988 ◽  
Vol 72 (4) ◽  
pp. 1316-1323 ◽  
Author(s):  
CA Sieff ◽  
CM Niemeyer ◽  
SJ Mentzer ◽  
DV Faller
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Messenger Rna ◽  
Tumor Necrosis ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Mesenchymal Cells ◽  
Colony Stimulating Factors ◽  
Gm Csf ◽  
Necrosis Factor

Abstract Although the genes for four hematopoietic colony-stimulating factors (CSFs) have been cloned, neither the mechanism of the regulation of their production nor their cellular origins have been established with certainty. Monocytes are known to produce colony-stimulating and burst- promoting activities, as well as several monokines such as interleukin- 1 (IL-1) and tumor necrosis factor (TNF). These monokines indirectly stimulate other mesenchymal cells to produce certain colony-stimulating factors such as granulocyte-macrophage CSF (GM-CSF). To determine whether monocytes produce other CSFs and if so, to compare the mechanism of regulation of production with that of endothelial cells and fibroblasts, we investigated the synthesis of CSFs by monocytes, human umbilical vein endothelial cells, and fibroblasts. We used total cellular RNA blot analysis to determine interleukin-3 (IL-3), GM-CSF, granulocyte CSF (G-CSF), and monocyte CSF (M-CSF) messenger RNA (mRNA) content and immunoprecipitation or bioassay to confirm the presence of the specific secreted proteins. The results indicate that M-CSF mRNA and protein are produced constitutively by all three cell types and their level of expression does not increase after induction. In contrast, GM-CSF and G-CSF mRNAs are barely detectable in uninduced monocytes and show an increase in expression after lipopolysaccharide treatment. Retrovirus-immortalized endothelial cells, unlike primary endothelial cells or both primary and immortalized fibroblasts, produce IL-1 constitutively; this correlates with their constitutive production of GM-CSF and G-CSF. IL-3 mRNA was not detectable in any of these cells either before or after induction. The results indicate that these mesenchymal cells can produce three CSFs: GM-CSF, G-CSF, and M-CSF; furthermore, the data suggest that the mechanism of regulation of M-CSF production is different from that of GM-CSF and G-CSF, and that the latter two inducible CSFs are regulated by different factors in monocytes compared with the other mesenchymal cells.

Shear stress increases endothelial platelet-derived growth factor mRNA levels

1991 ◽  
Vol 260 (2) ◽  
pp. H642-H646 ◽  
Author(s):  
H. J. Hsieh ◽  
N. Q. Li ◽  
J. A. Frangos
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Growth Factor ◽  
Umbilical Vein ◽  
Fold Increase ◽  
Platelet Derived Growth Factor ◽  
Mrna Levels ◽  
Cell Mitogen ◽  
Stress Dependent

We have investigated the effect of shear stress on platelet-derived growth factor (PDGF) A and B chain mRNA levels in cultured human umbilical vein endothelial cells (hUVEC). The levels of both PDGF A and B mRNA in hUVEC were increased by a physiological shear stress (16 dyn/cm2), reaching a maximum approximately 1.5-2 h after the onset of shear stress and returning almost to control values at 4 h. The peak levels showed a more than 10-fold enhancement for PDGF A mRNA and a 2- to 3-fold increase for PDGF B mRNA (P less than 0.05). PDGF A mRNA also showed a shear-dependent increase from 0 to 6 dyn/cm2 (P less than 0.05) and then plateaued from 6 to 51 dyn/cm2. PDGF B mRNA levels were elevated as shear stress increased from 0 to 6 dyn/cm2 then declined gradually to a minimum at 31 dyn/cm2 (P less than 0.05) and increased again when shear stress rose to 51 dyn/cm2 (P less than 0.05). PDGF, a potent smooth muscle cell mitogen and vasoconstrictor, released from the endothelium may regulate the blood flow in vivo. The shear stress-dependent elevation of PDGF A and B mRNA in endothelial cells may be involved in the adaptation of blood vessels to flow mediated by the endothelium.

The mitogenic activity of the liver growth factor is mediated by tumor necrosis factor alpha in rat liver

2003 ◽  
Vol 38 (5) ◽  
pp. 598-604 ◽  
Author(s):  
Juan J Dı́az-Gil ◽  
Pedro L Majano ◽  
Manuel López-Cabrera ◽  
Vicente Sánchez-López ◽  
Carmen Rúa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Rat Liver ◽  
Tumor Necrosis ◽  
Mitogenic Activity ◽  
Necrosis Factor Alpha ◽  
Liver Growth ◽  
Factor Alpha ◽  
Necrosis Factor
Sign in / Sign up

Export Citation Format

Share Document