scholarly journals Dominant effect of gap junction communication in wound‐induced calcium‐wave, NFAT activation and wound closure in keratinocytes

2021 ◽  
Author(s):  
Laura Hudson ◽  
Malcolm Begg ◽  
Blythe Wright ◽  
Tim Cheek ◽  
Colin A. B. Jahoda ◽  
...  
Keyword(s):  
Gap Junction ◽  
Wound Closure ◽  
Calcium Wave ◽  
Dominant Effect ◽  
Gap Junction Communication ◽  
Nfat Activation

scholarly journals The Sleep-inducing Lipid Oleamide Deconvolutes Gap Junction Communication and Calcium Wave Transmission in Glial Cells

1997 ◽  
Vol 139 (7) ◽  
pp. 1785-1792 ◽  
Author(s):  
Xiaojun Guan ◽  
Benjamin F. Cravatt ◽  
George R. Ehring ◽  
James E. Hall ◽  
Dale L. Boger ◽  
...  
Keyword(s):  
Gap Junction ◽  
Glial Cells ◽  
Wave Transmission ◽  
Calcium Wave ◽  
Mediated Communication ◽  
Gap Junctional Communication ◽  
Gap Junction Communication ◽  
Junctional Communication ◽  
Nervous System Function ◽  
Gap Junctional

Oleamide is a sleep-inducing lipid originally isolated from the cerebrospinal fluid of sleep-deprived cats. Oleamide was found to potently and selectively inactivate gap junction–mediated communication between rat glial cells. In contrast, oleamide had no effect on mechanically stimulated calcium wave transmission in this same cell type. Other chemical compounds traditionally used as inhibitors of gap junctional communication, like heptanol and 18β-glycyrrhetinic acid, blocked not only gap junctional communication but also intercellular calcium signaling. Given the central role for intercellular small molecule and electrical signaling in central nervous system function, oleamide- induced inactivation of glial cell gap junction channels may serve to regulate communication between brain cells, and in doing so, may influence higher order neuronal events like sleep induction.

scholarly journals Dynamic changes in β-cell [Ca2+] regulates NFAT activation, gene transcription and islet gap junction communication

2021 ◽  
pp. 101430
Author(s):  
Jose G. Miranda ◽  
Wolfgang E. Schleicher ◽  
Kristen L. Wells ◽  
David G. Ramirez ◽  
Samantha P. Landgrave ◽  
...  
Keyword(s):  
Gap Junction ◽  
Gene Transcription ◽  
Β Cell ◽  
Dynamic Changes ◽  
Gap Junction Communication ◽  
Nfat Activation

scholarly journals A Cell-Based High-Throughput Assay for Gap Junction Communication Suitable for Assessing Connexin 43–Ezrin Interaction Disruptors Using IncuCyte ZOOM

2016 ◽  
Vol 22 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Aleksandra R. Dukic ◽  
David W. McClymont ◽  
Kjetil Taskén
Keyword(s):  
Gap Junction ◽  
High Throughput ◽  
Connexin 43 ◽  
General Mechanism ◽  
Protein Protein Interaction ◽  
Gap Junction Communication ◽  
Anchoring Protein ◽  
A Cell ◽  
Rat Liver Epithelial Cells ◽  
High Throughput Assay

Connexin 43 (Cx43), the predominant gap junction (GJ) protein, directly interacts with the A-kinase-anchoring protein (AKAP) Ezrin in human cytotrophoblasts and a rat liver epithelial cells (IAR20). The Cx43-Ezrin–protein kinase (PKA) complex facilitates Cx43 phosphorylation by PKA, which triggers GJ opening in cytotrophoblasts and IAR20 cells and may be a general mechanism regulating GJ intercellular communication (GJIC). Considering the importance of Cx43 GJs in health and disease, they are considered potential pharmaceutical targets. The Cx43-Ezrin interaction is a protein-protein interaction that opens possibilities for targeting with peptides and small molecules. For this reason, we developed a high-throughput cell-based assay in which GJIC can be assessed and new compounds characterized. We used two pools of IAR20 cells, calcein loaded and unloaded, that were mixed and allowed to attach. Next, GJIC was monitored over time using automated imaging via the IncuCyte imager. The assay was validated using known GJ inhibitors and anchoring peptide disruptors, and we further tested new peptides that interfered with the Cx43-Ezrin binding region and reduced GJIC. Although an AlphaScreen assay can be used to screen for Cx43-Ezrin interaction inhibitors, the cell-based assay described is an ideal secondary screen for promising small-molecule hits to help identify the most potent compounds.

scholarly journals Propagation Distance of the α-Particle-Induced Bystander Effect: The Role of Nuclear Traversal and Gap Junction Communication

2009 ◽  
Vol 171 (5) ◽  
pp. 513-520 ◽  
Author(s):  
Sylvain Gaillard ◽  
David Pusset ◽  
Sonia M. de Toledo ◽  
Michel Fromm ◽  
Edouard I. Azzam
Keyword(s):  
Gap Junction ◽  
Bystander Effect ◽  
Propagation Distance ◽  
Gap Junction Communication

General Anesthetics Inhibit Gap Junction Communication in Cultured Organotypic Hippocampal Slices

2006 ◽  
Vol 102 (6) ◽  
pp. 1692-1698 ◽  
Author(s):  
Kirsten Wentlandt ◽  
Marina Samoilova ◽  
Peter L. Carlen ◽  
Hossam El Beheiry
Keyword(s):  
Gap Junction ◽  
Hippocampal Slices ◽  
General Anesthetics ◽  
Gap Junction Communication

Inhibiting N-cadherin-mediated adhesion affects gap junction communication in isolated rat hearts

2010 ◽  
Vol 30 (3) ◽  
pp. 193-200 ◽  
Author(s):  
Hongjun Zhu ◽  
Hegui Wang ◽  
Xiwen Zhang ◽  
Xiaofeng Hou ◽  
Kejiang Cao ◽  
...  
Keyword(s):  
Gap Junction ◽  
Gap Junction Communication ◽  
Rat Hearts ◽  
Isolated Rat

scholarly journals Effective protection of rabbits’ explosive brain injury through blocking gap junction communication

2013 ◽  
Vol 12 (4) ◽  
Author(s):  
Z Yong-Ming ◽  
L Jia-Chuan ◽  
Y Yan-Yan ◽  
S Wen-Jiang ◽  
T Hong ◽  
...  
Keyword(s):  
Brain Injury ◽  
Gap Junction ◽  
Effective Protection ◽  
Gap Junction Communication

scholarly journals Gap Junction–mediated Cell–Cell Communication Modulates Mouse Neural Crest Migration

1998 ◽  
Vol 143 (6) ◽  
pp. 1725-1734 ◽  
Author(s):  
G.Y. Huang ◽  
E.S. Cooper ◽  
K. Waldo ◽  
M.L. Kirby ◽  
N.B. Gilula ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Neural Crest ◽  
Gap Junction ◽  
Heart Defects ◽  
Neural Crest Cells ◽  
Dominant Negative ◽  
Cardiac Neural Crest ◽  
Gap Junction Communication ◽  
Neural Crest Migration

Previous studies showed that conotruncal heart malformations can arise with the increase or decrease in α1 connexin function in neural crest cells. To elucidate the possible basis for the quantitative requirement for α1 connexin gap junctions in cardiac development, a neural crest outgrowth culture system was used to examine migration of neural crest cells derived from CMV43 transgenic embryos overexpressing α1 connexins, and from α1 connexin knockout (KO) mice and FC transgenic mice expressing a dominant-negative α1 connexin fusion protein. These studies showed that the migration rate of cardiac neural crest was increased in the CMV43 embryos, but decreased in the FC transgenic and α1 connexin KO embryos. Migration changes occurred in step with connexin gene or transgene dosage in the homozygous vs. hemizygous α1 connexin KO and CMV43 embryos, respectively. Dye coupling analysis in neural crest cells in the outgrowth cultures and also in the living embryos showed an elevation of gap junction communication in the CMV43 transgenic mice, while a reduction was observed in the FC transgenic and α1 connexin KO mice. Further analysis using oleamide to downregulate gap junction communication in nontransgenic outgrowth cultures showed that this independent method of reducing gap junction communication in cardiac crest cells also resulted in a reduction in the rate of crest migration. To determine the possible relevance of these findings to neural crest migration in vivo, a lacZ transgene was used to visualize the distribution of cardiac neural crest cells in the outflow tract. These studies showed more lacZ-positive cells in the outflow septum in the CMV43 transgenic mice, while a reduction was observed in the α1 connexin KO mice. Surprisingly, this was accompanied by cell proliferation changes, not in the cardiac neural crest cells, but in the myocardium— an elevation in the CMV43 mice vs. a reduction in the α1 connexin KO mice. The latter observation suggests that cardiac neural crest cells may have a role in modulating growth and development of non–neural crest– derived tissues. Overall, these findings suggest that gap junction communication mediated by α1 connexins plays an important role in cardiac neural crest migration. Furthermore, they indicate that cardiac neural crest perturbation is the likely underlying cause for heart defects in mice with the gain or loss of α1 connexin function.

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