Nuclear translocation of fibroblast growth factor during Xenopus mesoderm induction

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 487-493 ◽  
Author(s):  
R.A. Shiurba ◽  
N. Jing ◽  
T. Sakakura ◽  
S.F. Godsave

Mesoderm induction, the earliest inductive cell-cell interaction in vertebrate embryogenesis, is thought to be mediated by polypeptide growth factors including fibroblast growth factor (FGF). Here we present an immunocytochemical analysis of FGF during mesoderm induction in Xenopus laevis. Antibodies to both basic and acidic FGF were immunoreactive with oocytes and early embryos. Immunostaining was predominantly intracellular and was concentrated in the marginal zone and vegetal pole throughout cleavage and blastula stages. In addition, basic FGF (bFGF) antibodies showed intense nuclear staining in these regions, at and following the mid-blastula transition, when embryonic transcription begins. Acidic FGF (aFGF) also appeared in some nuclei at these stages. Taken together the evidence suggests that FGF is prepositioned in mesoderm-forming regions and is actively involved in mesoderm induction in vivo.

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.


2018 ◽  
Vol 33 (6) ◽  
pp. 808-818 ◽  
Author(s):  
Jiankui Li ◽  
Xi Chen ◽  
Kaijian Ling ◽  
Zhiqing Liang ◽  
Huicheng Xu

Introduction and hypothesis: Pelvic support structure injury is the major cause of pelvic organ prolapse. At present, polypropylene-based filler material has been suggested as a common method to treat pelvic organ prolapse. However, it cannot functionally rehabilitate the pelvic support structure. In addition to its poor long-term efficiency, the urinary bladder matrix was the most suitable biological scaffold material for pelvic floor repair. Here, we hypothesize that anti-sca-1 monoclonal antibody and basic fibroblast growth factor were cross-linked to urinary bladder matrix to construct a two-factor bioscaffold for pelvic reconstruction. Methods Through a bispecific cross-linking reagent, sulfosuccinimidyl 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (sulfo-smcc) immobilized anti-sca-1 and basic fibroblast growth factor to urinary bladder matrix. Then scanning electron microscope and plate reader were used to detect whether the anti-sca-1/basic fibroblast growth factor-urinary bladder matrix scaffold was built successfully. After that, the capacity of enriching sca-1 positive cells was measured both in vitro and in vivo. In addition, we evaluated the differentiation capacity and biocompatibility of the scaffold. Finally, western blotting was used to detect the level of fibulin-5 protein. Results The scanning electron microscope and plate reader revealed that the double-factor biological scaffold was built successfully. The scaffold could significantly enrich a large number of sca-1 positive cells both in vitro and in vivo, and obviously accelerate cells and differentiate functional tissue with good biocompatibility. Moreover, the western blotting showed that the scaffold could improve the expression of fibulin-5 protein. Conclusion The anti-sca-1/basic fibroblast growth factor-urinary bladder matrix scaffold revealed good biological properties and might serve as an ideal scaffold for pelvic reconstruction.


10.1038/77548 ◽  
2000 ◽  
Vol 6 (7) ◽  
pp. 812-815 ◽  
Author(s):  
Yvonne P. Tretter ◽  
Moritz Hertel ◽  
Barbara Munz ◽  
Gerrit ten Bruggencate ◽  
Sabine Werner ◽  
...  

2014 ◽  
Vol 224 (3) ◽  
pp. 289-301 ◽  
Author(s):  
Aijun Zhang ◽  
Douglas H Sieglaff ◽  
Jean Philippe York ◽  
Ji Ho Suh ◽  
Stephen D Ayers ◽  
...  

Thyroid hormone (TH) acts through specific receptors (TRs), which are conditional transcription factors, to induce fibroblast growth factor 21 (FGF21), a peptide hormone that is usually induced by fasting and that influences lipid and carbohydrate metabolism via local hepatic and systemic endocrine effects. While TH and FGF21 display overlapping actions when administered, including reductions in serum lipids, according to the current models these hormones act independentlyin vivo. In this study, we examined mechanisms of regulation of FGF21 expression by TH and tested the possibility that FGF21 is required for induction of hepatic TH-responsive genes. We confirm that active TH (triiodothyronine (T3)) and the TRβ-selective thyromimetic GC1 increase FGF21 transcript and peptide levels in mouse liver and that this effect requires TRβ. T3also induces FGF21 in cultured hepatocytes and this effect involves direct actions of TRβ1, which binds a TRE within intron 2 of FGF21. Gene expression profiles of WT andFgf21-knockout mice are very similar, indicating that FGF21 is dispensable for the majority of hepatic T3gene responses. A small subset of genes displays diminished T3response in the absence of FGF21. However, most of these are not obviously directly involved in T3-dependent hepatic metabolic processes. Consistent with these results, T3-dependent effects on serum cholesterol are maintained in theFgf21−/−background and we observe no effect of theFgf21-knockout background on serum triglycerides and glucose. Our findings indicate that T3regulates the genes involved in classical hepatic metabolic responses independently of FGF21.


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