E-CADHERIN EXPRESSION CAN ALTER THE SPECIFICITY OF GAP JUNCTION FORMATION

1997 ◽  
Vol 21 (12) ◽  
pp. 833-843 ◽  
Author(s):  
D PROWSE
Keyword(s):  
Gap Junction ◽  
Junction Formation ◽  
E Cadherin

Dynamics of connexins, E-cadherin and alpha-catenin on cell membranes during gap junction formation

1997 ◽  
Vol 110 (3) ◽  
pp. 311-322 ◽  
Author(s):  
K. Fujimoto ◽  
A. Nagafuchi ◽  
S. Tsukita ◽  
A. Kuraoka ◽  
A. Ohokuma ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Gap Junction ◽  
Immunofluorescence Microscopy ◽  
Immunogold Electron Microscopy ◽  
Cell Contact ◽  
Contact Sites ◽  
Junction Formation ◽  
Intramembrane Proteins ◽  
Junction Proteins ◽  
E Cadherin

We examined the dynamics of connexins, E-cadherin and alpha-catenin during gap-junction disassembly and assembly in regeneration hepatocytes by immunofluorescence microscopy, and immunogold-electron microscopy using SDS-digested freeze-replicas. The present findings suggest that during the disappearance of gap junctions most of the gap junction plaques are broken up into smaller aggregates, and then the gap junction proteins may be removed from the cell membrane, but some of the connexons or connexins remain dispersed in the plane of membrane as pure morphologically indistinguishable intramembrane proteins. Double-immunogold electron microscopy using a polyclonal antibody for connexins and a monoclonal antibody for E-cadherin or alpha-catenin revealed co-localization of these molecules at cell-to-cell contact sites during the reappearance of gap junction plaques. This implies that, at least in regenerating hepatocytes, the cadherin-catenin complex-mediated cell-to-cell contact sites act as foci for gap junction formation. In addition, connexin-immunoreactivity was also observed along tight junctional strands, suggesting that the gap junction may also form along the tight junctions.

Cell adhesion and gap junction formation in the early mouse embryo are induced prematurely by 6-DMAP in the absence of E-cadherin phosphorylation

1994 ◽  
Vol 107 (5) ◽  
pp. 1369-1379 ◽  
Author(s):  
J. Aghion ◽  
C. Gueth-Hallonet ◽  
C. Antony ◽  
D. Gros ◽  
B. Maro
Keyword(s):  
Gap Junction ◽  
Mouse Embryo ◽  
Kinase Inhibitor ◽  
Post Translational Modification ◽  
Serine Threonine Kinase ◽  
Cell Stage ◽  
Surface Polarization ◽  
Junction Formation ◽  
Early Mouse ◽  
E Cadherin

Compaction of the mouse embryo, which takes place at the 8-cell stage, is dependent upon the adhesion molecule E-cadherin (uvomurulin), but does not require protein synthesis, suggesting that post-translational modification(s) is (are) implicated in the setting up of this phenomenon. The demonstration recently that E-cadherin is phosphorylated at the 8-cell stage just before compaction supports this theory. In this work we used 6-dimethylaminopurine, a serine-threonine kinase inhibitor, to investigate the role of protein phosphorylation in compaction of mouse embryos. 6-dimethylaminopurine is able to induce cell flattening and gap junction formation prematurely at the 4-cell stage; however, it does not induce cell surface polarization, as occurs during normal compaction. 6-dimethylaminopurine-induced premature flattening is inhibited when the embryos are cultured in the presence of an anti-E-cadherin antibody or without extra-cellular Ca2+, demonstrating that this process requires functional E-cadherin; whereas cell flattening and gap junction formation take place in the absence of E-cadherin phosphorylation, suggesting that its phosphorylation is not required normally for these events. The relationship between E-cadherin-mediated cell flattening and gap junction formation during compaction is discussed.

scholarly journals Opening Hemichannels in Nonjunctional Membrane Stimulates Gap Junction Formation

2004 ◽  
Vol 86 (2) ◽  
pp. 781-796 ◽  
Author(s):  
Derek L. Beahm ◽  
James E. Hall
Keyword(s):  
Gap Junction ◽  
Junction Formation

Control of gap junction formation in canine trachea by arachidonic acid metabolites

1986 ◽  
Vol 250 (3) ◽  
pp. C495-C505 ◽  
Author(s):  
R. Agrawal ◽  
E. E. Daniel
Keyword(s):  
Arachidonic Acid ◽  
Gap Junctions ◽  
Gap Junction ◽  
Direct Effects ◽  
Leukotriene C4 ◽  
Lipoxygenase Pathway ◽  
Junction Formation ◽  
Acid Metabolites ◽  
Pg E2

This study examined whether the synthesis of the metabolites of arachidonic acid (AA) was involved in gap junction formation by 4-aminopyridine (4-AP) treatment in vitro in canine trachealis. Studies were made of the effects on gap junction formation of putative inhibitors of the cyclooxygenase and of both this and the lipoxygenase pathway of AA metabolism and the direct effects of prostaglandins (PG) E2 and I2. The number of gap junctions of similar size was increased after brief exposure to 4-AP. After indomethacin (IDM), 4-AP treatment decreased the number of gap junctions but did not affect their size. Pretreatment with 5,8,11,14-eicosatetraynoic acid or nordihydroguiaretic acid, putative inhibitors of cyclooxygenase and lipoxygenase enzymes, inhibited both the 4-AP-induced increase and decrease in the number of gap junctions. FPL 55712, a putative antagonist of leukotriene C4, did not alter either the number or the size of gap junctions when added alone or in combination with IDM. AA alone increased the number of gap junctions, but after IDM, AA decreased the number of gap junctions compared with the controls. Incubation of trachealis strips in vitro for 30 min with PGE2 increased the number of gap junctions by about threefold along with an increase in the size of the gap junctions. Similar incubation with PGI2, however, increased the number of gap junctions by approximately 60% without any change in the size. In the course of some control experiments, an interaction between carbachol and alcohol was observed such that alcohol caused an IDM-sensitive relaxation of carbachol-induced contractions, which was not observed when serotonin was the contractile agent. These results strongly suggest that PGE2 and PGI2 increase the formation of gap junctions in canine trachealis and that these prostanoids are released by 4-AP treatment. Leukotrienes may also be inhibitory in the formation of gap junctions, but FPL 55712 did not affect either the increase or the decrease in gap junctions after 4-AP.

Membrane Perturbations and Mediation of Gap Junction Formation in Response to Taurine Treatment in Normal and Injured Alveolar Epithelia

1989 ◽  
Vol 15 (6) ◽  
pp. 895-908 ◽  
Author(s):  
Ronald E. Gordon ◽  
Richard F. Heller ◽  
J. Robert Del Valle ◽  
Rachael F. Heller
Keyword(s):  
Gap Junction ◽  
Junction Formation ◽  
Taurine Treatment

scholarly journals NLR-1/CASPR Anchors F-Actin to Promote Gap Junction Formation

2020 ◽  
Vol 55 (5) ◽  
pp. 574-587.e3
Author(s):  
Lingfeng Meng ◽  
Dong Yan
Keyword(s):  
Gap Junction ◽  
Junction Formation

Effects of inactivation of oxytocin receptor and inhibition of prostaglandin synthesis on uterine oxytocin receptor and gap junction formation and labor in the rat

1991 ◽  
Vol 69 (9) ◽  
pp. 1262-1267 ◽  
Author(s):  
W. Y. Chan ◽  
Irene Berezin ◽  
E. E. Daniel ◽  
K. C. Russell ◽  
Victor J. Hruby
Keyword(s):  
Gap Junction ◽  
Naproxen Sodium ◽  
Critical Role ◽  
Treated Group ◽  
Oxytocin Receptor ◽  
Prostaglandin Synthesis ◽  
Pregnant Rats ◽  
Junction Formation ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Oxytocin Antagonist

Normal term labor is associated with a surge in myometrial oxytocin receptor formation and gap junction development. We have previously shown that inhibition of prostaglandin synthesis by naproxen sodium, 2.0 mg/day, suppressed oxytocin receptor formation but not gap junction formation and prolonged gestation. In this study, we investigated the effects of a specific oxytocin antagonist on oxytocin receptor formation, gap junction formation, and labor in the rat. [Pen1Phe(Me)2,Thr4,Orn8]oxytocin, a specific oxytocin antagonist, was infused subcutaneously during the last 3 days of pregnancy at 300 μg/day. Measurements of myometrial oxytocin receptor concentrations and gap junction formation on days 21 and 22 and days 22–23 (in labor) pregnant uteri showed no significant differences in the Bmax and Kd values between the control and the treated group. Gestation period was not prolonged by the oxytocin antagonist. However, in a separate group of day 23 pregnant rats, the uterine contractile response to 60 mU of oxytocin i.v. was found completely blocked by 10 μg of the oxytocin antagonist. These findings suggest that although functional oxytocin receptors did not appear to be essential for the initiation of labor, oxytocin antagonists may still be effective in the prevention of premature contractions. We also examined the effects of a higher dose of naproxen sodium, 5.0 mg/day, on gap junction formation. At this dose, naproxen sodium suppressed both oxytocin receptor and gap junction formation, prolonged gestation, and delayed parturition by 24 h or longer. Prostaglandin appears to be an important regulator or mediator of oxytocin receptor and gap junction formation and plays a critical role in the initiation of labor.Key words: oxytocin, prostaglandin, oxytocin receptor, gap junction, labor.

Sign in / Sign up

Export Citation Format

Share Document