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.

Gap junction formation and regulation in myometrium

1980 ◽  
Vol 239 (5) ◽  
pp. C217-C228 ◽  
Author(s):  
R. E. Garfield ◽  
D. Merrett ◽  
A. K. Grover
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
High Frequency ◽  
Actinomycin D ◽  
Low Frequency ◽  
Synthesis Inhibitor ◽  
Pregnant Rats ◽  
Junction Formation ◽  
Prostacyclin Analog

Myometrial tissues from pregnant rats were examined by electron microscopy for the presence of gap junctions after incubation in vitro with a variety of agents. Gap junctions were present in low frequency or absent prior to incubation in vitro. The junctions were present in control tissues in high frequency after 48 h incubation. The addition of cycloheximide or actinomycin D inhibited the incorporation of [3H]leucine into TCA-precipitable proteins and prevented gap junction formation. A prostacyclin analog (carbacyclin), a thromboxane synthesis inhibitor, and indomethacin also prevented gap junction formation. Oxytocin had no effect on gap junction formation but isoxsuprine decreased their number and increased their size. Isoxsuprine and isoproterenol also produced electron opaque crystals associated with the gap junctions. Dibutyryl cAMP treatment but not monobutyryl cGMP also increased the size of gap junctions. Based upon this and previous studies, we propose at least four sites for regulation of gap junctions and possible control of labor.

Arachidonic acid metabolites issued from the lipoxygenase pathway and lymphocyte response in vitro

1982 ◽  
Vol 4 (4) ◽  
pp. 353
Author(s):  
N. Gualde ◽  
H. Rabinovitch-Chable ◽  
M. Rigaud ◽  
M. Fredon ◽  
J. Durand ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Lymphocyte Response ◽  
Lipoxygenase Pathway ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Rapid de novo formation of gap junctions between insect hemocytes in vitro: a freeze-fracture, dye- transfer and patch-clamp study

1993 ◽  
Vol 104 (3) ◽  
pp. 763-772 ◽  
Author(s):  
D. Churchill ◽  
S. Coodin ◽  
R. R. Shivers ◽  
S. Caveney
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Periplaneta Americana ◽  
Single Channel ◽  
De Novo ◽  
Freeze Fracture ◽  
Cell Contact ◽  
Junction Formation ◽  
Insect Hemocytes

Gap junctions form between insect hemocytes (blood cells) when they encapsulate foreign objects in the hemocoel (body cavity). In this study we show that hemocytes from cockroach (Periplaneta americana) form gap-junctions rapidly in vitro. Freeze-fracture replicas of hemocyte aggregates fixed 5 minutes after bleeding contain gap-junctional plaques. Dye passage was detected between carboxyfluorescein diacetate- labelled and unlabelled hemocytes within 3 minutes of bleeding, when the cells made contact as they flattened rapidly onto coverslips. When double whole-cell voltage-clamp was used to measure gap-junction formation between cells which were pushed together, electrical coupling was detected within one second of cell-cell contact. To prevent extensive flattening, cells were plated onto lipophorin-coated coverslips. Junctional conductance increased in staircase fashion with steps corresponding to an average single channel conductance of 345 pS. Assuming all channels to have this conductance, the maximal accretion rate of channels to the growing junction was one channel per second. Junctional currents and dye-coupling were detected in the absence of Ca2+, indicating that involvement of Ca2+-dependent adhesion molecules is not a prerequisite for gap-junction formation in hemocytes. Hemocytes from distantly related insects (cockroach and moth) form functional gap junctions with each other, suggesting sequence homology among gap- junction proteins in insects. The function of rapid gap-junction formation between hemocytes during encapsulation and wound healing in vivo are discussed.

scholarly journals Two Drosophila Innexins Are Expressed in Overlapping Domains and Cooperate to Form Gap-Junction Channels

2000 ◽  
Vol 11 (7) ◽  
pp. 2459-2470 ◽  
Author(s):  
Lucy A. Stebbings ◽  
Martin G. Todman ◽  
Pauline Phelan ◽  
Jonathan P. Bacon ◽  
Jane A. Davies
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Ectopic Expression ◽  
In Vivo Studies ◽  
Electrophysiological Properties ◽  
Gap Junction Channels ◽  
Overlapping Domains ◽  
In Vitro Data

Members of the innexin protein family are structural components of invertebrate gap junctions and are analogous to vertebrate connexins. Here we investigate two Drosophila innexin genes,Dm-inx2 and Dm-inx3 and show that they are expressed in overlapping domains throughout embryogenesis, most notably in epidermal cells bordering each segment. We also explore the gap-junction–forming capabilities of the encoded proteins. In pairedXenopus oocytes, the injection of Dm-inx2mRNA results in the formation of voltage-sensitive channels in only ∼ 40% of cell pairs. In contrast, Dm-Inx3 never forms channels. Crucially, when both mRNAs are coexpressed, functional channels are formed reliably, and the electrophysiological properties of these channels distinguish them from those formed by Dm-Inx2 alone. We relate these in vitro data to in vivo studies. Ectopic expression ofDm-inx2 in vivo has limited effects on the viability ofDrosophila, and animals ectopically expressingDm-inx3 are unaffected. However, ectopic expression of both transcripts together severely reduces viability, presumably because of the formation of inappropriate gap junctions. We conclude that Dm-Inx2 and Dm-Inx3, which are expressed in overlapping domains during embryogenesis, can form oligomeric gap-junction channels.

Arachidonic acid metabolites induced β-adrenoceptor densitization in rat lung in vitro

1985 ◽  
Vol 30 (5) ◽  
pp. 799-809 ◽  
Author(s):  
Luisa Daffonchio ◽  
Maria Pia Abbracchio ◽  
Alicia Hernandez ◽  
Emanuela Giani ◽  
Flaminio Cattabeni ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Rat Lung ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Sharp Wave-Like Activity in the Hippocampus In Vitro in Mice Lacking the Gap Junction Protein Connexin 36

2003 ◽  
Vol 89 (4) ◽  
pp. 2046-2054 ◽  
Author(s):  
Isabel Pais ◽  
Sheriar G. Hormuzdi ◽  
Hannah Monyer ◽  
Roger D. Traub ◽  
Ian C. Wood ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Frequency Oscillation ◽  
Connexin 36 ◽  
Sharp Wave ◽  
Bath Application ◽  
Junction Protein ◽  
Gap Junction Protein ◽  
Electrical Signaling

Bath application of kainate (100–300 nM) induced a persistent gamma-frequency (30–80 Hz) oscillation that could be recorded in stratum radiatum of the CA3 region in vitro. We have previously described that in knockout mice lacking the gap junction protein connexin 36 (Cx36KO), γ-frequency oscillations are reduced but still present. We now demonstrate that in the Cx36KO mice, but not in wild-type (WT), large population field excitatory postsynaptic potentials, or sharp wave-burst discharges, also occurred during the on-going γ-frequency oscillation. These spontaneous burst discharges were not seen in WT mice. Burst discharges in the Cx36KO mice occurred with a mean frequency of 0.23 ± 0.11 Hz and were accompanied by a series of fast (approximately 60–115 Hz) population spikes or “ripple” oscillations in many recordings. Intracellular recordings from CA3 pyramidal cells showed that the burst discharges consisted of a depolarizing response and presumed coupling potentials (spikelets) could occasionally be seen either before or during the burst discharge. The burst discharges occurring in Cx36KO mice were sensitive to gap junctions blockers as they were fully abolished by carbenoxolone (200 μM). In control mice we made several attempts to replicate this pattern of sharp wave activity/ripples occurring with the on-going kainate-evoked γ-frequency oscillation by manipulating synaptic and electrical signaling. Partial disruption of inhibition, in control slices, by bath application of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (1–4 μM) completely abolished all γ-frequency activity before any burst discharges occurred. Increasing the number of open gap junctions in control slices by using trimethylamine (TMA; 2–10 mM), in conjunction with kainate, failed to elicit any sharp wave bursts or fast ripples. However, bath application of the potassium channel blocker 4-aminopyridine (4-AP; 20–80 μM) produced a pattern of activity in control mice (13/16 slices), consisting of burst discharges occurring in conjunction with kainate-evoked γ-frequency oscillations, that was similar to that seen in Cx36KO mice. In a few cases ( n = 9) the burst discharges were accompanied by fast ripple oscillations. Carbenoxolone also fully blocked the 4-AP-evoked burst discharges ( n = 5). Our results show that disruption of electrical signaling in the interneuronal network can, in the presence of kainate, lead to the spontaneous generation of sharp wave/ripple activity similar to that observed in vivo. This suggests a complex role for electrically coupled interneurons in the generation of hippocampal network activity.

scholarly journals The Functional Implications of Endothelial Gap Junctions and Cellular Mechanics in Vascular Angiogenesis

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 237 ◽  
Author(s):  
Takayuki Okamoto ◽  
Haruki Usuda ◽  
Tetsuya Tanaka ◽  
Koichiro Wada ◽  
Motomu Shimaoka
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Gap Junctions ◽  
Gap Junction ◽  
Cancer Cells ◽  
Tumor Development ◽  
Tube Formation ◽  
Cellular Mechanics

Angiogenesis—the sprouting and growth of new blood vessels from the existing vasculature—is an important contributor to tumor development, since it facilitates the supply of oxygen and nutrients to cancer cells. Endothelial cells are critically affected during the angiogenic process as their proliferation, motility, and morphology are modulated by pro-angiogenic and environmental factors associated with tumor tissues and cancer cells. Recent in vivo and in vitro studies have revealed that the gap junctions of endothelial cells also participate in the promotion of angiogenesis. Pro-angiogenic factors modulate gap junction function and connexin expression in endothelial cells, whereas endothelial connexins are involved in angiogenic tube formation and in the cell migration of endothelial cells. Several mechanisms, including gap junction function-dependent or -independent pathways, have been proposed. In particular, connexins might have the potential to regulate cell mechanics such as cell morphology, cell migration, and cellular stiffness that are dynamically changed during the angiogenic processes. Here, we review the implication for endothelial gap junctions and cellular mechanics in vascular angiogenesis.

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