scholarly journals Connexin Hemichannels and Gap Junction Channels Are Differentially Influenced by Lipopolysaccharide and Basic Fibroblast Growth Factor

2007 ◽  
Vol 18 (1) ◽  
pp. 34-46 ◽  
Author(s):  
Elke De Vuyst ◽  
Elke Decrock ◽  
Marijke De Bock ◽  
Hiroshi Yamasaki ◽  
Christian C. Naus ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Growth Factor ◽  
Gap Junction ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cell Communication ◽  
Atp Release ◽  
Arachidonic Acid Metabolism ◽  
C6 Glioma Cells ◽  
Fibroblast Growth

Gap junction (GJ) channels are formed by two hemichannels (connexons), each contributed by the cells taking part in this direct cell–cell communication conduit. Hemichannels that do not interact with their counterparts on neighboring cells feature as a release pathway for small paracrine messengers such as nucleotides, glutamate, and prostaglandins. Connexins are phosphorylated by various kinases, and we compared the effect of various kinase-activating stimuli on GJ channels and hemichannels. Using peptides identical to a short connexin (Cx) amino acid sequence to specifically block hemichannels, we found that protein kinase C, Src, and lysophosphatidic acid (LPA) inhibited GJs and hemichannel-mediated ATP release in Cx43-expressing C6 glioma cells (C6-Cx43). Lipopolysaccharide (LPS) and basic fibroblast growth factor (bFGF) inhibited GJs, but they stimulated ATP release via hemichannels in C6-Cx43. LPS and bFGF inhibited hemichannel-mediated ATP release in HeLa-Cx43 cells, but they stimulated it in HeLa-Cx43 with a truncated carboxy-terminal (CT) domain or in HeLa-Cx26, which has a very short CT. Hemichannel potentiation by LPS was inhibited by blockers of the arachidonic acid metabolism, and arachidonic acid had a potentiating effect like LPS and bFGF. We conclude that GJ channels and hemichannels display similar or oppositely directed responses to modulatory influences, depending on the balance between kinase activity and the activity of the arachidonic acid pathway. Distinctive hemichannel responses to pathological stimulation with LPS or bFGF may serve to optimize the cell response, directed at strictly controlling cellular ATP release, switching from direct GJ communication to indirect paracrine signaling, or maximizing cell-protective strategies.

Arachidonic acid mediates calcium influx induced by basic fibroblast growth factor in Balb-c 3T3 fibroblasts

Cell Calcium ◽  
1997 ◽  
Vol 22 (3) ◽  
pp. 179-188 ◽  
Author(s):  
Luca Munaron ◽  
Susanna Antoniotti ◽  
Carla Distasi ◽  
Davide Lovisolo
Keyword(s):  
Arachidonic Acid ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Calcium Influx ◽  
Fibroblast Growth ◽  
3T3 Fibroblasts

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.

Cell-to-Cell Communication and Expression of Gap Junctional Proteins in Human Diabetic and Nondiabetic Skin Fibroblasts: Effects of Basic Fibroblast Growth Factor

Endocrine ◽  
1999 ◽  
Vol 10 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Kay M. Abdullah ◽  
Girish Luthra ◽  
Jerzy J. Bilski ◽  
S. Ahmed Abdullah ◽  
Lawrence P. Reynolds ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cell Communication ◽  
Skin Fibroblasts ◽  
Fibroblast Growth ◽  
Junctional Proteins ◽  
Gap Junctional

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.

C6 Glioma Cells Produce Basic Fibroblast Growth Factor That Can Stimulate Their Own Proliferation

1989 ◽  
Vol 106 (5) ◽  
pp. 904-909 ◽  
Author(s):  
Nobuaki Okumura ◽  
Kouichi Takimoto ◽  
Masato Okada ◽  
Hachiro Nakagawa
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Glioma Cells ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Fibroblast Growth
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