scholarly journals Fibroblast Growth Factor 4 Directs Gap Junction Expression in the Mesenchyme of the Vertebrate Limb Bud

1997 ◽  
Vol 138 (5) ◽  
pp. 1125-1137 ◽  
Author(s):  
H. Makarenkova ◽  
D.L. Becker ◽  
C. Tickle ◽  
A.E. Warner
Keyword(s):  
Growth Factor ◽  
Gap Junctions ◽  
Gap Junction ◽  
Fibroblast Growth Factor ◽  
Connexin 43 ◽  
Limb Bud ◽  
Functional Coupling ◽  
Fibroblast Growth ◽  
Mesenchyme Cells

Pattern in the developing limb depends on signaling by polarizing region mesenchyme cells, which are located at the posterior margin of the bud tip. Here we address the underlying cellular mechanisms. We show in the intact bud that connexin 43 (Cx43) and Cx32 gap junctions are at higher density between distal posterior mesenchyme cells at the tip of the bud than between either distal anterior or proximal mesenchyme cells. These gradients disappear when the apical ectodermal ridge (AER) is removed. Fibroblast growth factor 4 (FGF4) produced by posterior AER cells controls signaling by polarizing cells. We find that FGF4 doubles gap junction density and substantially improves functional coupling between cultured posterior mesenchyme cells. FGF4 has no effect on cultured anterior mesenchyme, suggesting that any effects of FGF4 on responding anterior mesenchyme cells are not mediated by a change in gap junction density or functional communication through gap junctions. In condensing mesenchyme cells, connexin expression is not affected by FGF4. We show that posterior mesenchyme cells maintained in FGF4 under conditions that increase functional coupling maintain polarizing activity at in vivo levels. Without FGF4, polarizing activity is reduced and the signaling mechanism changes. We conclude that FGF4 regulation of cell–cell communication and polarizing signaling are intimately connected.

scholarly journals Transforming Growth Factor-β3 Increases Gap-Junctional Communication among Folliculostellate Cells to Release Basic Fibroblast Growth Factor

Endocrinology ◽  
2005 ◽  
Vol 146 (9) ◽  
pp. 4054-4060 ◽  
Author(s):  
Nurul Kabir ◽  
Kirti Chaturvedi ◽  
Lian Sheng Liu ◽  
Dipak K. Sarkar
Keyword(s):  
Growth Factor ◽  
Gap Junction ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Connexin 43 ◽  
Fibroblast Growth ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional ◽  
Gap Junction Inhibitor

Abstract Folliculostellate (FS) cells are known to communicate with each other and with endocrine cells via gap junctions in the anterior pituitary. We investigated whether TGFβ3 and estradiol, known to regulate FS cell production and secretion of basic fibroblast growth factor (bFGF), increases gap junctional communication to alter bFGF secretion from FS cells. FS cells in monolayer cultures were treated with TGFβ3 or vehicle alone for 24 h and then microinjected with Lucifer Yellow and high-molecular-weight Texas Red dextran. Ten minutes later the transfer of dye among adjacent cells was recorded with a digital microscope. TGFβ3 increased the transfer of dye. The TGFβ3-neutralizing antibody and the gap junction inhibitor octanol reduced the effect of TGFβ3 on the transfer of dye. The TGFβ3-induced transfer of dye was unaltered by simultaneous treatment with estradiol. The steroid alone also had no effect. TGFβ3 increased total and phosphorylated levels of connexin 43. Estradiol treatment did not produce any significant changes on basal or TGFβ3-induced increases in connexin 43 levels. The gap-junction inhibitor octanol reduced TGFβ3-increased levels of bFGF in FS cells. Taken together, these results suggest that TGFβ3 may act on FS cells to increase gap-junctional communication to maximize its effect on bFGF secretion.

Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth muscle

2009 ◽  
Vol 297 (1) ◽  
pp. F46-F54 ◽  
Author(s):  
Masaaki Imamura ◽  
Hiromitsu Negoro ◽  
Akihiro Kanematsu ◽  
Shingo Yamamoto ◽  
Yu Kimura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Gap Junction ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Connexin 43 ◽  
Muscle Layer ◽  
Fibroblast Growth ◽  
Cholinergic Agonist ◽  
Junction Protein

Overactive bladder is a highly prevalent clinical condition that is often caused by bladder outlet obstruction (BOO). Increased coupling of bladder smooth muscle cells (BSMC) via gap junctions has been hypothesized as a mechanism for myogenic bladder overactivity in BOO, although little is known about the regulatory system underlying such changes. Here, we report the involvement of basic fibroblast growth factor (bFGF) and connexin 43, a bladder gap junction protein, in bladder overactivity. BOO created by urethral constriction in rats resulted in elevated bFGF and connexin 43 levels in the bladder urothelium and muscle layer, respectively, and muscle strips from these bladders were more sensitive than those from sham-operated controls to a cholinergic agonist. In vitro bFGF treatment increased connexin 43 expression in cultured rat BSMC via the ERK 1/2 pathway. This finding was supported by another in vivo model, where bFGF released from gelatin hydrogels fixed on rat bladder walls caused connexin 43 upregulation and gap junction formation in the muscle layer. Bladder muscle strips in this model showed increased sensitivity to a cholinergic agonist that was blocked by inhibition of gap junction function with α-glycyrrhetinic acid. Cystometric analyses of this model showed typical features of detrusor overactivity such as significantly increased micturition frequency and decreased bladder capacity. These findings suggest that bFGF from the urothelium could induce bladder hypersensitivity to acetylcholine via gap junction generation in the smooth muscle, thereby contributing to the myogenic overactivity of obstructed bladders.

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 Biochemical and ultrastructural evidence for the association of basic fibroblast growth factor with cardiac gap junctions.

1991 ◽  
Vol 266 (29) ◽  
pp. 19551-19557
Author(s):  
E. Kardami ◽  
R.M. Stoski ◽  
B.W. Doble ◽  
T. Yamamoto ◽  
E.L. Hertzberg ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gap Junctions ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Ultrastructural Evidence

Evaluation of the bioactivity about anti-sca-1/basic fibroblast growth factor-urinary bladder matrix scaffold for pelvic reconstruction

2018 ◽  
Vol 33 (6) ◽  
pp. 808-818 ◽  
Author(s):  
Jiankui Li ◽  
Xi Chen ◽  
Kaijian Ling ◽  
Zhiqing Liang ◽  
Huicheng Xu
Keyword(s):  
Growth Factor ◽  
Urinary Bladder ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Pelvic Organ ◽  
Fibroblast Growth ◽  
Pelvic Reconstruction ◽  
Urinary Bladder Matrix

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.

Induction of activin A is essential for the neuroprotective action of basic fibroblast growth factor in vivo

10.1038/77548 ◽  
2000 ◽  
Vol 6 (7) ◽  
pp. 812-815 ◽  
Author(s):  
Yvonne P. Tretter ◽  
Moritz Hertel ◽  
Barbara Munz ◽  
Gerrit ten Bruggencate ◽  
Sabine Werner ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Activin A ◽  
Fibroblast Growth ◽  
Neuroprotective Action
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