Intercellular communication and tissue growth: VIII. A genetic analysis of junctional communication and cancerous growth

1977 ◽  
Vol 34 (1) ◽  
pp. 1-27 ◽  
Author(s):  
R. Azarnia ◽  
W. R. Loewenstein
Keyword(s):  
Genetic Analysis ◽  
Intercellular Communication ◽  
Tissue Growth ◽  
Junctional Communication

scholarly journals INTERCELLULAR COMMUNICATION AND TISSUE GROWTH

1967 ◽  
Vol 33 (2) ◽  
pp. 235-242 ◽  
Author(s):  
Werner R. Loewenstein ◽  
Richard D. Penn
Keyword(s):  
Intercellular Communication ◽  
Wound Closure ◽  
Cell Movement ◽  
Normal Growth ◽  
Tissue Growth ◽  
Cellular Communication ◽  
Mechanical Contact ◽  
Cell Systems ◽  
Intact State ◽  
Striking Contrast

Intercellular communication was examined in regenerating rat liver and urodele skin, two tissues of fast but normal growth. In both, cellular communication is in general as good as in their respective normal intact state. This stands in striking contrast to the lack of cellular communication in tissues with cancerous growth. Upon wounding of the urodele skin, the normally permeable junctional membranes of cells near the wound border seal themselves off, thereby insulating the interiors of the communicated cell systems from the exterior. When the cells of two opposing borders make mechanical contact in the course of wound closure, communication between them ensues within 30 min. Within this period all cell movement also ceases ("contact inhibition"). The possible implications of these findings in the control of tissue growth are discussed.

scholarly journals PI3k and Stat3: Oncogenes that are Required for Gap Junctional, Intercellular Communication

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 167 ◽  
Author(s):  
Mulu Geletu ◽  
Zaid Taha ◽  
Patrick T. Gunning ◽  
Leda Raptis
Keyword(s):  
Intercellular Communication ◽  
Single Cells ◽  
Survival Function ◽  
Phosphatidyl Inositol ◽  
Transformed Cells ◽  
Gap Junctional Intercellular Communication ◽  
Junctional Communication ◽  
Human Lung Carcinoma ◽  
Mutational Activation ◽  
Gap Junctional

Gap junctional, intercellular communication (GJIC) is interrupted in cells transformed by oncogenes such as activated Src. The Src effector, Ras, is required for this effect, so that Ras inhibition restores GJIC in Src-transformed cells. Interestingly, the inhibition of the Src effector phosphatidyl-inositol-3 kinase (PI3k) or Signal Transducer and Activator of Transcription-3 (Stat3) pathways does not restore GJIC. In the contrary, inhibition of PI3k or Stat3 in non-transformed rodent fibroblasts or epithelial cells or certain human lung carcinoma lines with extensive GJIC inhibits communication, while mutational activation of PI3k or Stat3 increases GJIC. Therefore, it appears that oncogenes such as activated Src have a dual role upon GJIC; acting as inhibitors of communication through the Ras pathway, and as activators through activation of PI3k or Stat3. In the presence of high Src activity the inhibitory functions prevail so that the net effect is gap junction closure. PI3k and Stat3 constitute potent survival signals, so that their inhibition in non-transformed cells triggers apoptosis which, in turn, has been independently demonstrated to suppress GJIC. The interruption of gap junctional communication would confine the apoptotic event to single cells and this might be essential for the maintenance of tissue integrity. We hypothesize that the GJIC activation by PI3k or Stat3 may be linked to their survival function.

scholarly journals Enhanced Secretion of Amylase from Exocrine Pancreas of Connexin32-deficient Mice

1998 ◽  
Vol 141 (5) ◽  
pp. 1267-1275 ◽  
Author(s):  
Marc Chanson ◽  
Marjorie Fanjul ◽  
Domenico Bosco ◽  
Eric Nelles ◽  
Susanne Suter ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Intercellular Communication ◽  
Plaque Assay ◽  
Acinar Cells ◽  
Pancreatic Acinar Cells ◽  
Amylase Secretion ◽  
Wild Type ◽  
Patch Clamp Recording ◽  
Junctional Communication

To determine whether junctional communication between pancreatic acinar cells contributes to their secretory function in vivo, we have compared wild-type mice, which express the gap junctional proteins connexin32 (Cx32) and connexin26, to mice deficient for the Cx32 gene. Pancreatic acinar cells from Cx32 (−/−) mice failed to express Cx32 as evidenced by reverse transcription–PCR and immunolabeling and showed a marked reduction (4.8- and 25-fold, respectively) in the number and size of gap junctions. Dye transfer studies showed that the extent of intercellular communication was inhibited in Cx32 (−/−) acini. However, electrical coupling was detected by dual patch clamp recording in Cx32 (−/−) acinar cell pairs. Although wild-type and Cx32 (−/−) acini were similarly stimulated to release amylase by carbamylcholine, Cx32 (−/−) acini showed a twofold increase of their basal secretion. This effect was caused by an increase in the proportion of secreting acini, as detected with a reverse hemolytic plaque assay. Blood measurements further revealed that Cx32 (−/−) mice had elevated basal levels of circulating amylase. The results, which demonstrate an inverse relationship between the extent of acinar cell coupling and basal amylase secretion in vivo, support the view that the physiological recruitment of secretory acinar cells is regulated by gap junction mediated intercellular communication.

Connexin mimetic peptides: specific inhibitors of gap-junctional intercellular communication

2001 ◽  
Vol 29 (4) ◽  
pp. 606-612 ◽  
Author(s):  
W. H. Evans ◽  
S. Boitano
Keyword(s):  
Gap Junctions ◽  
Intercellular Communication ◽  
Gap Junctional Intercellular Communication ◽  
Reversible Inhibitors ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Wide Range ◽  
Mimetic Peptides ◽  
Gap Junctional ◽  
Specific Sequences

Intercellular co-operation is a fundamental and widespread feature in tissues and organs. An important mechanism ensuring multicellular homoeostasis involves signalling between cells via gap junctions that directly connect the cytosolic contents of adjacent cells. Cell proliferation and intercellular communication across gap junctions are closely linked, and a number of pathologies in which communication is disrupted are known where connexins, the gap-junctional proteins, are modified. The proteins of gap junctions thus emerge as therapeutic targets inviting the development and exploitation of chemical tools and drugs that specifically influence intercellular communication. Connexin mimetic peptides that correspond to short specific sequences in the two extracellular loops of connexins are a class of benign, specific and reversible inhibitors of gap-junctional communication that have been studied recently in a broad range of cells, tissues and organs. This review summarizes the properties and uses of these short synthetic peptides, and compares their probable mechanism of action with those of a wide range of other less specific traditional gap-junction inhibitors.

scholarly journals Wounding alters epidermal connexin expression and gap junction-mediated intercellular communication.

1995 ◽  
Vol 6 (11) ◽  
pp. 1491-1501 ◽  
Author(s):  
J A Goliger ◽  
D L Paul
Keyword(s):  
Intercellular Communication ◽  
Wound Repair ◽  
Lucifer Yellow ◽  
Dye Transfer ◽  
Connexin Expression ◽  
Differentiated Cells ◽  
Junctional Communication ◽  
Patterns Of Communication ◽  
In Cells

We show that connexin expression and in vivo patterns of communication were dramatically altered in response to epidermal wounding. Six hours after injury, Cx26 was up-regulated in the differentiated cells proximal to the wound, but was down-regulated in cells located at the wound edge. In contrast, Cx31.1 and Cx43 were down-regulated in cells both peripheral to and at the wounded edge. These patterns of altered connexin expression were detectable as early as 2 h after wounding and were most pronounced in 24-h old wounds. Increased expression of Cx26 was still evident in the hyperproliferative epidermis of 6-day old wounds. In vivo dye transfer experiments with Lucifer yellow and neurobiotin confirmed that junctional communication patterns were altered in ways consistent with changes in connexin expression. The data thus suggest that intercellular communication is intimately involved in regulating epidermal wound repair.

scholarly journals INTERCELLULAR COMMUNICATION AND TISSUE GROWTH

1968 ◽  
Vol 38 (3) ◽  
pp. 556-561 ◽  
Author(s):  
A. Jamakosmanović ◽  
W. R. Loewenstein
Keyword(s):  
Intercellular Communication ◽  
Tissue Growth ◽  
Membrane Potentials ◽  
Normal Cells ◽  
Thyroid Cancers ◽  
Normal Thyroid

Intercellular communication was examined in normal and cancerous isolated thyroids with an intracellular electrical technique. The cells of normal thyroid (rat, mouse, hamster, man) communicate, within any given follicle, through permeable junctions. The cells of a wide variety of thyroid cancers (rat, hamster) do not communicate to any detectable degree and have resting membrane potentials lower than those of normal cells.

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