In vivo and in vitro localization of brain-derived neurotrophic factor, fibroblast growth factor-2 and their receptors in the bullfrog vestibular end organs

2002 ◽  
Vol 102 (1-2) ◽  
pp. 83-99 ◽  
Author(s):  
Ricardo Cristobal ◽  
Paul Popper ◽  
Ivan Lopez ◽  
Paul Micevych ◽  
Jean De Vellis ◽  
...  
2009 ◽  
Vol 106 (17) ◽  
pp. 7191-7196 ◽  
Author(s):  
Beatrice Paradiso ◽  
Peggy Marconi ◽  
Silvia Zucchini ◽  
Elena Berto ◽  
Anna Binaschi ◽  
...  

A loss of neurons is observed in the hippocampus of many patients with epilepsies of temporal lobe origin. It has been hypothesized that damage limitation or repair, for example using neurotrophic factors (NTFs), may prevent the transformation of a normal tissue into epileptic (epileptogenesis). Here, we used viral vectors to locally supplement two NTFs, fibroblast growth factor–2 (FGF-2) and brain-derived neurotrophic factor (BDNF), when epileptogenic damage was already in place. These vectors were first characterized in vitro, where they increased proliferation of neural progenitors and favored their differentiation into neurons, and they were then tested in a model of status epilepticus-induced neurodegeneration and epileptogenesis. When injected in a lesioned hippocampus, FGF-2/BDNF expressing vectors increased neuronogenesis, embanked neuronal damage, and reduced epileptogenesis. It is concluded that reduction of damage reduces epileptogenesis and that supplementing specific NTFs in lesion areas represents a new approach to the therapy of neuronal damage and of its consequences.


Author(s):  
Eishin Yaoita ◽  
Masaaki Nameta ◽  
Yutaka Yoshida ◽  
Hidehiko Fujinaka

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.


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

2016 ◽  
Vol 130 (9) ◽  
pp. 667-681 ◽  
Author(s):  
Szu-Yu Chien ◽  
Chun-Yin Huang ◽  
Chun-Hao Tsai ◽  
Shih-Wei Wang ◽  
Yu-Min Lin ◽  
...  

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.


The Prostate ◽  
1994 ◽  
Vol 25 (4) ◽  
pp. 206-209 ◽  
Author(s):  
Jack Geller ◽  
Lida R. Sionit ◽  
Andrew Baird ◽  
Matthew Kohls ◽  
Kenneth M. Connors ◽  
...  

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

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