Fibroblast growth factor-2 induces stromelysin-1 (MMP3) expression in endothelial cells by activating mitogen-activated protein kinases

2000 ◽  
Vol 191 (4) ◽  
pp. S37
Author(s):  
Christopher C. Derivaux ◽  
Giuseppe Pintucci ◽  
Pay-Jen Yu ◽  
Eric Silver ◽  
Graziano Seghezzi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Protein Kinases ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein

scholarly journals Cell Density-Dependent Fibroblast Growth Factor-2 Signaling Regulates Syndecan-4 Expression in Cultured Vascular Endothelial Cells

2020 ◽  
Vol 21 (10) ◽  
pp. 3698 ◽  
Author(s):  
Takato Hara ◽  
Shiori Yabushita ◽  
Chika Yamamoto ◽  
Toshiyuki Kaji
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Heparan Sulfate ◽  
Fibroblast Growth Factor ◽  
Cell Density ◽  
Vascular Endothelial Cells ◽  
Fibroblast Growth Factor 2 ◽  
Vascular Endothelial ◽  
Fibroblast Growth ◽  
Density Dependent

Syndecan-4 is a member of the syndecan family of transmembrane heparan sulfate proteoglycans, and is involved in cell protection, proliferation, and the blood coagulation-fibrinolytic system in vascular endothelial cells. Heparan sulfate chains enable fibroblast growth factor-2 (FGF-2) to form a complex with its receptor and to transduce the cell growth signal. In the present study, bovine aortic endothelial cells were cultured, and the intracellular signal pathways that mediate the regulation of syndecan-4 expression in dense and sparse cultures by FGF-2 were analyzed. We demonstrated the cell density-dependent differential regulation of syndecan-4 expression. Specifically, we found that FGF-2 upregulated the synthesis of syndecan-4 in vascular endothelial cells via the MEK1/2-ERK1/2 pathway in dense cell cultures, with only a transcriptional induction of syndecan-4 at a low cell density via the Akt pathway. This study highlights a critical mechanism underlying the regulation of endothelial cell functions by proteoglycans.

scholarly journals Changes in fibroblast growth factor 2 and its receptors in bovine follicles before and after GnRH application and after ovulation

Reproduction ◽  
2006 ◽  
Vol 131 (2) ◽  
pp. 319-329 ◽  
Author(s):  
Bajram Berisha ◽  
Martin Steffl ◽  
Werner Amselgruber ◽  
Dieter Schams
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Corpora Lutea ◽  
Fibroblast Growth ◽  
Lh Surge ◽  
Short Period ◽  
Before And After ◽  
Capillary Endothelial Cells

The aim of this study was to evaluate the expression pattern of fibroblast growth factor 2 (FGF2), its receptor variants (FGFR1IIIc, FGFR2IIIc) and nucleolin in time-defined follicle classes before and after GnRH application and after ovulation in the cow. Ovaries containing preovulatory follicles or new corpora lutea (CL) were collected at approximately 0, 4, 10, 20 and 25 h (follicles) and 60 h (new CL) relative to injection of GnRH to induce an LH surge (n= 5 animals per group). The expressions of FGF2 and FGFR1IIIc mRNA were significantly up-regulated only in the follicle group 4 h after GnRH (during the LH surge) with a significant down-regulation immediately afterwards. Western blot analyses showed two protein bands with at 22 and 18 kDa with apparent up-regulation beginning with the LH surge (4 h) and maximum levels 20 h after GnRH. FGF2 protein in follicles collected at 0 h (before LH surge) was localised in theca tissue (endothelial and pericytes of blood vessels) but not in granulosa cells (GCs). The FGF2 staining (by immunohistochemistry) pattern changed dramatically after the LH surge for a short period (about 2 days) and FGF2 protein was localised dominantly in the nucleus of many GCs, while most capillary endothelial cells were FGF2 immunonegative. In conclusion, the novel observation of FGF2 up-regulation and the distinct change in FGF2 localisation from theca (cytoplasm of endothelial cells) to the nucleus of GCs after the LH surge may be important for survival of GCs or for the transition of the GCs to luteal cells.

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