Lindane Inhibition of Gap Junctional Communication in Myometrial Myocytes Is Partially Dependent on Phosphoinositide-Generated Second Messengers

1995 ◽  
Vol 130 (2) ◽  
pp. 280-293 ◽  
Author(s):  
K.A. Criswell ◽  
R. Lochcaruso ◽  
E.L. Stuenkel
Keyword(s):  
Second Messengers ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional

scholarly journals Regulation of connexin43 gap junctional communication by phosphatidylinositol 4,5-bisphosphate

2007 ◽  
Vol 177 (5) ◽  
pp. 881-891 ◽  
Author(s):  
Leonie van Zeijl ◽  
Bas Ponsioen ◽  
Ben N.G. Giepmans ◽  
Aafke Ariaens ◽  
Friso R. Postma ◽  
...  
Keyword(s):  
Second Messengers ◽  
Pdz Domain ◽  
Cell Communication ◽  
Receptor Activation ◽  
Gap Junctional Communication ◽  
Signaling Complex ◽  
Junctional Communication ◽  
Gap Junctional ◽  
Zona Occludens ◽  
Cell Cell

Cell–cell communication through connexin43 (Cx43)-based gap junction channels is rapidly inhibited upon activation of various G protein–coupled receptors; however, the mechanism is unknown. We show that Cx43-based cell–cell communication is inhibited by depletion of phosphatidylinositol 4,5-bisphosphate (PtdIns[4,5]P2) from the plasma membrane. Knockdown of phospholipase Cβ3 (PLCβ3) inhibits PtdIns(4,5)P2 hydrolysis and keeps Cx43 channels open after receptor activation. Using a translocatable 5-phosphatase, we show that PtdIns(4,5)P2 depletion is sufficient to close Cx43 channels. When PtdIns(4,5)P2 is overproduced by PtdIns(4)P 5-kinase, Cx43 channel closure is impaired. We find that the Cx43 binding partner zona occludens 1 (ZO-1) interacts with PLCβ3 via its third PDZ domain. ZO-1 is essential for PtdIns(4,5)P2-hydrolyzing receptors to inhibit cell–cell communication, but not for receptor–PLC coupling. Our results show that PtdIns(4,5)P2 is a key regulator of Cx43 channel function, with no role for other second messengers, and suggest that ZO-1 assembles PLCβ3 and Cx43 into a signaling complex to allow regulation of cell–cell communication by localized changes in PtdIns(4,5)P2.

Gap junction-mediated transfer of left-right patterning signals in the early chick blastoderm is upstream of Shh asymmetry in the node

Development ◽  
1999 ◽  
Vol 126 (21) ◽  
pp. 4703-4714 ◽  
Author(s):  
M. Levin ◽  
M. Mercola
Keyword(s):  
Gene Expression ◽  
Gap Junction ◽  
Large Scale ◽  
Chick Blastoderm ◽  
Gap Junction Channels ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Left And Right ◽  
The Right ◽  
Gap Junctional

Invariant patterning of left-right asymmetry during embryogenesis depends upon a cascade of inductive and repressive interactions between asymmetrically expressed genes. Different cascades of asymmetric genes distinguish the left and right sides of the embryo and are maintained by a midline barrier. As such, the left and right sides of an embryo can be viewed as distinct and autonomous fields. Here we describe a series of experiments that indicate that the initiation of these programs requires communication between the two sides of the blastoderm. When deprived of either the left or the right lateral halves of the blastoderm, embryos are incapable of patterning normal left-right gene expression at Hensen's node. Not only are both flanks required, suggesting that there is no single signaling source for LR pattern, but the blastoderm must be intact. These results are consistent with our previously proposed model in which the orientation of LR asymmetry in the frog, Xenopus laevis, depends on large-scale partitioning of LR determinants through intercellular gap junction channels (M. Levin and M. Mercola (1998) Developmental Biology 203, 90–105). Here we evaluate whether gap junctional communication is required for the LR asymmetry in the chick, where it is possible to order early events relative to the well-characterized left and right hierarchies of gene expression. Treatment of cultured chick embryos with lindane, which diminishes gap junctional communication, frequently unbiased normal LR asymmetry of Shh and Nodal gene expression, causing the normally left-sided program to be recapitulated symmetrically on the right side of the embryo. A survey of early expression of connexin mRNAs revealed that Cx43 is present throughout the blastoderm at Hamburger-Hamilton stage 2–3, prior to known asymmetric gene expression. Application of antisense oligodeoxynucleotides or blocking antibody to cultured embryos also resulted in bilateral expression of Shh and Nodal transcripts. Importantly, the node and primitive streak at these stages lack Cx43 mRNA. This result, together with the requirement for an intact blastoderm, suggests that the path of communication through gap junction channels circumvents the node and streak. We propose that left-right information is transferred unidirectionally throughout the epiblast by gap junction channels in order to pattern left-sided Shh expression at Hensen's node.

Syncytial organization of cultured rat mesangial cells

1991 ◽  
Vol 260 (6) ◽  
pp. F848-F855 ◽  
Author(s):  
K. Iijima ◽  
L. C. Moore ◽  
M. S. Goligorsky
Keyword(s):  
Calcium Channels ◽  
Mesangial Cells ◽  
Calcium Waves ◽  
Oxygen Intermediates ◽  
Voltage Gated ◽  
Fura 2 ◽  
Gap Junctional Communication ◽  
Voltage Gated Calcium Channels ◽  
Junctional Communication ◽  
Gap Junctional

To investigate communication competence of cultured rat mesangial cells, Lucifer yellow transfer was studied using microinjection and scrape-loading techniques. Both methods yielded results indicating considerable gap junctional communication between cultured mesangial cells. Gap junctional communication between mesangial cells was upregulated by adenosine 3',5'-cyclic monophosphate (cAMP). Conversely, cell-to-cell communication was attenuated by exposure to the tumor promoter phorbol myristate acetate, the Ca ionophore ionomycin, reduced oxygen intermediates, and cell acidification. Expression of voltage gated calcium channels by mesangial cells was studied microspectrofluorimetrically using fura-2 fluorescence. KCl-induced depolarization, BAY-K 8644, and readdition of calcium to Ca-free depolarizing medium all produced a nifedipine-inhibitable increase in cytosolic calcium concentration. The existence of voltage-gated calcium channels in communication-competent cells suggests the possibility of propagation of depolarizing signals across the syncytium. This was studied by microapplication of KCl to the microenvironment of a single cell and monitoring fura-2 fluorescence in remote cells. This maneuver resulted in propagating calcium waves in communication-competent monolayers; calcium waves could not be evoked in monolayers exposed to an alkanol-type gap junction uncoupler, octanol. It is concluded that cultured rat mesangial cells form a syncytium capable of propagating calcium transients from a single depolarized cell to its coupled neighbors.

scholarly journals Hyperglycaemia and Diabetes Impair Gap Junctional Communication among Astrocytes

ASN NEURO ◽  
2010 ◽  
Vol 2 (2) ◽  
pp. AN20090048 ◽  
Author(s):  
Gautam K Gandhi ◽  
Kelly K Ball ◽  
Nancy F Cruz ◽  
Gerald A Dienel
Keyword(s):  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional

High glucose promotes gap junctional communication in cultured neonatal cardiac fibroblasts via AMPK activation

2014 ◽  
Vol 48 (4) ◽  
pp. 599-606 ◽  
Author(s):  
F. Chen ◽  
W. -T. Zhao ◽  
F. -X. Chen ◽  
G. -S. Fu ◽  
Y. Mou ◽  
...  
Keyword(s):  
High Glucose ◽  
Cardiac Fibroblasts ◽  
Ampk Activation ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Gap Junctional
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