scholarly journals Interleukin-1β induces fibroblast growth factor 2 expression and subsequently promotes endothelial progenitor cell angiogenesis in chondrocytes

2016 ◽  
Vol 130 (9) ◽  
pp. 667-681 ◽  
Author(s):  
Szu-Yu Chien ◽  
Chun-Yin Huang ◽  
Chun-Hao Tsai ◽  
Shih-Wei Wang ◽  
Yu-Min Lin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Neutralizing Antibody ◽  
Interleukin 1Β ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

Angiogenesis is an important event in the process of arthritis. Stimulating chondrocytes with IL-1β increased the expression of FGF-2, via the IL-1RI/ROS/AMPK/p38/NF-κB signalling pathway. FGF-2-neutralizing antibody abolished ATDC5-conditional medium-mediated angiogenesis both in vitro and in vivo.

scholarly journals Dynamic changes of podocytes caused by fibroblast growth factor 2 in culture

2021 ◽  
Author(s):  
Eishin Yaoita ◽  
Masaaki Nameta ◽  
Yutaka Yoshida ◽  
Hidehiko Fujinaka
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Quiescent State ◽  
Fibroblast Growth ◽  
Gene Expressions ◽  
Dynamic Changes ◽  
Ki 67

AbstractFibroblast growth factor 2 (FGF2) augments podocyte injury, which induces glomerulosclerosis, although the mechanisms remain obscure. In this study, we investigated the effects of FGF2 on cultured podocytes with interdigitating cell processes in rats. After 48 h incubation with FGF2 dynamic changes in the shape of primary processes and cell bodies of podocytes resulted in the loss of interdigitation, which was clearly shown by time-lapse photography. FGF2 reduced the gene expressions of constituents of the slit diaphragm, inflections of intercellular junctions positive for nephrin, and the width of the intercellular space. Immunostaining for the proliferation marker Ki-67 was rarely seen and weakly stained in the control without FGF2, whereas intensely stained cells were frequently found in the presence of FGF2. Binucleation and cell division were also observed, although no significant increase in cell number was shown. An in vitro scratch assay revealed that FGF2 enhanced migration of podocytes. These findings show that FGF2 makes podocytes to transition from the quiescent state into the cell cycle and change their morphology due to enhanced motility, and that the culture system in this study is useful for analyzing the pathological changes of podocytes in vivo.

scholarly journals Comparative Study In Vivo and In Vitro of Uniformly 14C-Labelled and 125I-Labelled Recombinant Fibroblast Growth Factor 2

1997 ◽  
Vol 249 (2) ◽  
pp. 473-480 ◽  
Author(s):  
Sylvie Colin ◽  
Frederic Mascarelli ◽  
Jean-Claude Jeanny ◽  
Raymond Vienet ◽  
Gerard Bouche ◽  
...  
Keyword(s):  
Growth Factor ◽  
Comparative Study ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

In vivo and in vitro effects of androgen on fibroblast growth factor-2 concentrations in the human prostate

The Prostate ◽  
1994 ◽  
Vol 25 (4) ◽  
pp. 206-209 ◽  
Author(s):  
Jack Geller ◽  
Lida R. Sionit ◽  
Andrew Baird ◽  
Matthew Kohls ◽  
Kenneth M. Connors ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Human Prostate ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
In Vitro Effects

scholarly journals Fibroblast Growth Factor 2 Drives Changes in Gene Expression Following Injury to Murine Cartilage In Vitro and In Vivo

2013 ◽  
Vol 65 (9) ◽  
pp. 2346-2355 ◽  
Author(s):  
Ka‐Wing Chong ◽  
Anastasios Chanalaris ◽  
Annika Burleigh ◽  
Huilin Jin ◽  
Fiona E. Watt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

scholarly journals Apoptosis of human glioma cells in vitro and in vivo induced by a neutralizing antibody against human basic fibroblast growth factor

1996 ◽  
Vol 85 (6) ◽  
pp. 1072-1077 ◽  
Author(s):  
Nozomu Murai ◽  
Tetsuya Ueba ◽  
Jun A. Takahashi ◽  
Hong-Qiong Yang ◽  
Haruhiko Kikuchi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Neutralizing Antibody ◽  
Fibroblast Growth ◽  
Human Glioma ◽  
Glioma Cell Lines

✓ Basic fibroblast growth factor (bFGF) is mitogenic to neuroectoderm- and mesoderm-derived cells and is a potent angiogenic factor. Abundant amounts of this factor and its receptor are detected in human glioma tissues and cells, and bFGF in glioma is thought to be involved in autonomous cell growth as an autocrine growth factor. A neutralizing mouse monoclonal antibody (MAb) against bFGF, 3H3 MAb, has been shown to inhibit both in vitro and in vivo growth of human glioma cell lines. This study shows that the human glioma cell lines U-87MG and U-251MG, which express high levels of bFGF and its receptor, can be induced to undergo apoptosis when cultured with 3H3 MAb. It is also demonstrated that 3H3 MAb can cause apoptosis in the same glioma cells that were transplanted into nude mice. Furthermore, enforced overexpression of bcl-2 protein by gene transfection prevented 3H3 MAb-induced apoptosis of glioma cells. It is concluded that induction of apoptosis by the neutralizing antibody is a promising therapeutic strategy for glioma.

In vivo angiogenic activity of urokinase: role of endogenous fibroblast growth factor-2

1999 ◽  
Vol 112 (23) ◽  
pp. 4213-4221
Author(s):  
D. Ribatti ◽  
D. Leali ◽  
A. Vacca ◽  
R. Giuliani ◽  
A. Gualandris ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Chorioallantoic Membrane ◽  
Fibroblast Growth Factor 2 ◽  
Dependent Manner ◽  
Fibroblast Growth ◽  
Angiogenic Activity ◽  
Amino Terminal

In vitro experimental evidences suggest that the proteolytic degradation of the extracellular matrix (ECM) by activation of the urokinase-type plasminogen activator (uPA)/plasmin system may affect growth factor activity and bioavailability. However, no direct in vivo observations were available to support this hypothesis. Here we demonstrate that endothelial GM 7373 cells overexpressing human uPA (uPA-R5 cells) cause the release of (125)I-labeled fibroblast growth factor-2 (FGF2) from endothelial ECM in a plasmin-dependent manner. Accordingly, uPA-R5 cells are angiogenic in vivo when applied on the top of the chorioallantoic membrane (CAM) of the chick embryo. In contrast, mock-transfected Neo2 cells are unable to release ECM-bound (125)I-FGF2 and are poorly angiogenic. Neovascularization elicited by uPA-R5 cells is significantly reduced by neutralizing anti-FGF2 antibodies to values similar to those observed in Neo2 cell-treated CAMs. Accordingly, purified human uPA stimulates neovascularization of the CAM in the absence of an inflammatory response. The angiogenic activity of uPA is significantly inhibited by neutralizing anti-FGF2 antibodies or by pretreatment with phenylmethylsulfonyl fluoride. The non-catalytic, receptor-binding amino-terminal fragment of uPA is instead non angiogenic. Taken together, the data indicate that uPA is able to induce angiogenesis in vivo via a plasmin-dependent degradation of ECM that causes the mobilization of stored endogenous FGF2.

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