Basic fibroblast growth factor stimulates connexin-43 expression and intercellular communication of cardiac fibroblasts

1995 ◽  
Vol 143 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Bradley W. Doble ◽  
Elissavet Kardami
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Cardiac Fibroblasts ◽  
Fibroblast Growth

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.

Antifibrotic response of cardiac fibroblasts in hypertensive hearts through enhanced TIMP-1 expression by basic fibroblast growth factor

2014 ◽  
Vol 23 (2) ◽  
pp. 92-100 ◽  
Author(s):  
Toshio Kinoshita ◽  
Yukio Ishikawa ◽  
Michitsune Arita ◽  
Yuri Akishima-Fukasawa ◽  
Kazuko Fujita ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cardiac Fibroblasts ◽  
Fibroblast Growth

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 Regulation of Connexin 43 by Basic Fibroblast Growth Factor in the Bladder: Transcriptional and Behavioral Implications

2011 ◽  
Vol 185 (6) ◽  
pp. 2398-2404 ◽  
Author(s):  
Hiromitsu Negoro ◽  
Akihiro Kanematsu ◽  
Masaaki Imamura ◽  
Yu Kimura ◽  
Ryosuke Matsuoka ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Connexin 43 ◽  
Fibroblast Growth
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