Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intercellular Junctions”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed2002

Connexin expression and gap junctional intercellular communication in human first trimester trophoblast.

Connexin (Cx) expression and gap junctional intercellular communication (GJIC) are involved in development and differentiation processes, and recently mutation of connexin genes has been implicated in pathologies. In the human placenta, two distinct differentiation pathways of cytotrophoblastic cells coexist and lead to a fusion phenotype (villous trophoblast) and a proliferative/invasive phenotype (extravillous trophoblast). Here we characterized in situ and in vitro the expression of Cx transcripts and proteins in the villous and extravillous trophoblast of first trimester placenta. In addition, the GJIC functionality was investigated using the gap-fluorescence recovery after photobleaching (gap-FRAP) method. We demonstrated in the villous trophoblast the presence of Cx43 mRNA and of Cx43 protein localized between cytotrophoblastic cells and between cytotrophoblastic cells and syncytiotrophoblast. In vitro, a transient functional gap junctional intertrophoblastic communication was demonstrated during the trophoblast fusion leading to the multinucleated syncytiotrophoblast. During the proliferative process of the extravillous trophoblast, Cx40 is expressed in the proximal part of the cell columns. When cytotrophoblastic cells were cultured on Matrigel for 2 days, alpha5beta1 integrin expression was observed concomitant with the presence of Cx40 mRNA and of Cx40 protein between the cells. No evidence for a GJIC was detected in this induced extravillous phenotype. In addition, Cx32 was detected between some aggregated cells after 72 h of culture. Our data show that the presence of Cx43 allows an inter-trophoblastic GJIC and is associated with the fusion process leading to the villous syncytiotrophoblast and that the presence of Cx40 does not allow GJIC and is associated with the extravillous phenotype.

Cell Communication↗
PubMed1982

Structure of intercellular junctions in different segments of the intrapulmonary vasculature.

Freeze-fracture studies have shown that there is a segmental differentiation of the structure of intercellular junctions of intraacinar pulmonary vessels. Tight junctions vary in complexity, being composed in the arterial segment of the most highly interconnected and most numerous (two to seven) rows of tight junction particles, which are present in E face grooves. In capillaries, they consist of one to three rows of particles, which, in the venular segment, show some discontinuities. Tight junctions in intraacinar veins consist of one to five rows of particles in the E face. Large gap junctions are numerous and are intimately associated with arterial tight junctions. They are absent from capillaries, and are fewer in number and smaller in size in veins than in arteries. The above observations suggest that, as in the systemic circulation, the venular segment is likely to be the most permeable to small, water-soluble solutes. The presence of numerous gap junctions, particularly in the arteries, suggests that in this segment there is a high degree of electrotonic and/or metabolic coupling between endothelial cells.

Animals↗
PubMed1992

Homologous and heterologous gap-junctional intercellular communication in v-raf-, v-myc-, and v-raf/v-myc-transduced rat liver epithelial cell lines.

We examined gap-junctional intercellular communication (GJIC) in a series of normal and v-raf-, v-myc-, and v-raf/v-myc-transduced rat liver epithelial (RLE) cell lines using the scrape loading-dye transfer and fluorescence-recovery-after-photobleaching (FRAP) assays. Whereas the normal RLE cell line, the control helper virus-transduced cell line, and the v-myc-transduced cell line all showed excellent GJIC, the v-raf-transduced cell lines displayed decreasing levels of GJIC associated with their increasing tumorigenicity. The v-raf/v-myc-transformed cell lines showed the lowest levels of GJIC and were also the most tumorigenic. Heterologous GJIC of these oncogene-transduced cell lines was also compared with that in the normal RLE cells. A modified FRAP assay, using fluorescent-microbead labelling to identify the oncogene-transduced cell from surrounding normal cells, was used to quantify the heterologous GJIC. The v-raf/v-myc-transformed RLE cells had no heterologous communication with the normal RLE cells, whereas v-raf- and v-myc-transduced cell lines maintained heterologous GJIC. Northern analysis showed that connexin 43 was the only gap-junction protein message expressed in these cell lines; connexin 32 and connexin 26 were not expressed. The levels of connexin 43 mRNA expression were relatively unchanged in all cell lines, suggesting that the reduction in GJIC was primarily at the posttranslational level. These findings suggest that reduction of homologous GJIC in v-raf- and v-raf/v-myc-transformed RLE cells is linked to their tumorigenic potential. Furthermore, the loss of heterologous GJIC, which we observed only in the v-raf/v-myc-transformed cells, might release such cells from the growth-regulating effects of surrounding normal cells, possibly contributing to their enhanced tumorigenic potential.

Actins↗
PubMed2003

Modulation of human fibroblast gap junction intercellular communication by hyaluronan.

The composition of the extracellular matrix changes during dermal repair. Initially, hyaluronan (HA) concentration is high, however, by day 3, HA is eliminated. HA optimizes collagen organization within granulation tissue. One possible mechanism of HA modulation of collagen packing is through the promotion of gap junction intercellular communication (GJIC). Gap junctions are gated channels that allow rapid intercellular communication and synchronization of coupled cell activities. The gap junction channel is composed of connexin (Cx) proteins that form a gated channel between coupled cells. HA is reported to enhance Cx43 expression in transformed fibroblasts. GJIC was quantified by the scrape loading technique and reported as a coupling index. The coupling index for human dermal fibroblasts was 4.6 +/- 0.2, while the coupling index for fibroblasts treated with HA more than doubled to 10.6 +/- 0.7. By Western blot analysis no differences were appreciated in the protein levels of Cx43 or beta-catenin, a protein involved in the translocation of Cx to the cell surface. By immuno-histology Cx43 and beta-catenin were evenly distributed throughout the cell in controls, but in cells treated with HA these proteins were co-localized to the cell surface. Coupled fibroblasts are reported to enhance the organization of collagen fibrils. It is proposed that HA increases the accumulation of Cx43 and beta-catenin on the cell surface, leading to greater GJIC and enhanced collagen organization.

Cell Communication↗
PubMed1994

Increased gap junctional intercellular communication in Syrian hamster embryo cells treated with oxidative agents.

The effects of K2CrO4, H2O2, benzoyl peroxide, menadione, KBrO3 and UV365nm on gap junctional intercellular communication (GJIC) have been studied in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-sensitive Syrian hamster embryo (SHE) cell line BPNi. All agents were found to increase the level of GJIC by 50-100%. Also, in early passage SHE cells, a tendency for increased GJIC was found for the oxidative agents studied. Hydrogen peroxide was used as a model compound in the subsequent studies. The increase in GJIC was reversible, and it was not due to an increased non-junctional permeability. Hydrogen peroxide counteracted the TPA-induced decrease in GJIC, regardless of whether the cells were exposed to the compounds simultaneously or the cells were pre-exposed to TPA before addition of H2O2. The GJIC enhancement by H2O2 was slightly reduced by the addition of the hydroxyl radical scavenger dimethylsulphoxide or by the inhibition of catalase by amitrole. The cAMP/protein kinase A system is the only characterized signal transduction system that is known to increase GJIC in most cell types. Hydrogen peroxide did not increase the amount of cAMP (or cGMP) in BPNi cells, while forskolin and a phosphodiesterase inhibitor had to increase the cAMP level several-fold to affect GJIC to the same degree as the oxidative agents. Some inhibitors of protein kinase A were assayed for their ability to inhibit the increases in GJIC caused by H2O2 and forskolin. Staurosporine inhibited the forskolin-induced increase in GJIC, with much less effect on the H2O2-induced increase. H8, H88 and H89 had less effect than staurosporine on the forskolin-induced increase in GJIC. The results suggest that the cAMP/protein kinase A system may not be involved in the increase in GJIC caused by H2O2, although this cannot be completely ruled out.

Animals↗
PubMed1989

Distribution and three-dimensional structure of intercellular junctions in canine myocardium.

Electrotonic coupling of cardiac myocytes at gap junctions may influence patterns of conduction in myocardium. To delineate the three-dimensional structure and distribution of intercellular junctions, we analyzed serial ultrathin sections of canine myocardium with transmission electron microscopy and disaggregated myocytes with scanning electron microscopy. Morphometric analysis of left ventricular myocardium sectioned in three orthogonal planes revealed that 80% of total gap junctional membrane occurred in large, ribbon-like gap junctions oriented transversely at cell end processes. The remaining 20% of gap junctional membrane was contained in small gap junctions located within plicate segments (interdigitating regions of cell-to-cell adhesion) of intercalated disks. In serial ultrathin sections, all gap junctions were contiguous with plicate segments. Thus, true "lateral" gap junctions do not exist in working ventricular myocytes and would not likely be able to withstand shear forces created by laterally sliding cells. Examination of serial plastic sections with light microscopy revealed complex overlapping of myocytes such that individual myocytes were connected at intercalated disks to an average of 9.1 +/- 2.2 other myocytes. These observations provide an improved understanding of the extent and distribution of cell junctions and should facilitate experimental and model studies of conduction in myocardium.

Animals↗
PubMed1984

Intercellular junctions in the hepatopancreas of the lobster Nephrops norvegicus.

The hepatopancreas of the lobster has recently been found to be a rich source of material from which to isolate arthopod gap junctions biochemically (Finbow et al., 1983a; 1984). It has therefore been studied here to assess the features of these intercellular junctions and any others that may be present, in vivo. The tissue consists of columnar epithelial cells which possess apical microvilli and basal infoldings. In thin sections the lateral borders of these cells are characterized by desmosomes and smooth septate junctions as well as by gap junctions. The desmosomes exhibit no apparent freeze fracture profile but the septate junctions display parallel rows of ridges or aligned intramembranous particles (IMPs) with complementary grooves on the other membrane half; these IMPs shift in their preferential fracturing plane depending on whether the tissue has first been fixed, always remaining on the EF if unfixed. The IMPs or connexons, of which the gap junctions are composed, fracture onto the E face, leaving complementary pits on the P face, regardless of whether the tissue is fixed or not. At the base of the pancreatic cells, the lateral borders are thrown into interdigitating folds which display endocytotic profiles and possible internalization of junction-bearing membranes. This phenomenon, which is readily visualized both after tracer incubation and in replicas, may represent junctional degradation relating to membrane turnover.

Animals↗
PubMed1990

Alterations of intercellular junctions induced by hypoxia in canine myocardium.

To delineate potential structural mechanisms of impaired cell coupling induced by hypoxia in canine myocardium, we characterized derangements in intercellular junctions and alterations in the space constant in strips of ventricular epimyocardium before and after selected intervals of hypoxia in vitro. Tissue samples were analyzed morphometrically with transmission and freeze-fracture electron microscopy. Space constants in control tissues averaged 1.61 +/- 0.47 mm (mean +/- SD). After 30 and 60 min of hypoxia, space constants declined by 0.24 +/- 0.22 and 0.32 +/- 0.17 mm, respectively (P less than 0.05 vs. control in each case). Impaired coupling was not reversible with reoxygenation. Focal pathological separation of intercalated disk membranes was observed after 30 min of hypoxia, but morphometric analysis demonstrated no reduction in gap junction surface density to account for uncoupling after 30 min of hypoxia. However, after 60 min of hypoxia, gap junction surface density was reduced by 45%. Quantitative analysis of freeze-fractured gap junction replicas after 30 min of hypoxia revealed a significant decrease in P-face particle diameter from 8.51 +/- 1.64 nm in control tissues to 7.25 +/- 1.33 nm (P less than 0.01) with no further change at 60 min. Thus impaired coupling at 30 min is likely related to a change in the gap junction particle. Further uncoupling after 60 min of hypoxia is likely related, in addition, to reduced gap junction surface density. These results suggest that alterations in P-face particles and gap junction surface density are important determinants of progressive cellular uncoupling induced by hypoxia.

Animals↗
PubMedDate not supplied

Single-channel currents of an intercellular junction.

We have used a double whole-cell patch-clamp system to make the first quantitative recordings of the single-channel current from an intercellular junction, presumably a gap junction. The junctional channel has various conductance states and discriminates poorly between cations and anions. It seems to change slowly from one conductance state to another.

Animals↗
PubMed1976

Fine structure of the rectum in cockroaches (Dictyoptera): general organization and intercellular junctions.

The organization of the rectal pads is described in cockroaches belonging to the Groups Blattoidea (Periplaneta americana, Blatta orientalis) and Blaberoidea (Supella supellectillu, Blaberus craniifer). In the Blattoidea, each pad is composed of two layers (principal and basal cells) and is surrounded by very narrow junctional cells supporting the sclerotized cuticle of the pad frame; basally, the junctional cells abut on to the basal cells. In the Blaberoidea, the basal cell layer is discontinuous, the basal cells being interspersed between extensions of the junctional cells beneath the pad. The ultrastructural features of each cell type is described, with special reference to the intercellular junctions, which exhibit unusual complexity. Four types of junction are recognized: desmosomes (belt and spot desmosomes), gap junctions, septate junctions and scalariform (ladder-like) junctions. The last are usually closely associated with mitochondria, forming mitochondrial-scalariform junction complexes (MS). The distribution of these junctions is examined in relation to the partitioning of extracellular spaces, and to the problem of fluid transport.

Animals↗
PubMed1976

Substructure of intercellular junctions in freeze-fractured alveolar-capillary membranes of mouse lung.

The purpose of this study was to examine by freeze-fracture the ultrastructure of intercellular junctions between mouse pulmonary endothelial and epithelial cells, and to relate this fine structure to that deduced from previous physiological and ultrastructural studies using tracer techniques. Junctions between capillary endothelial cells consist of one to three interconnected rows of particles which show occasional discontinuities. Small gap junctions are associated with these rows of particles in the arteriolar end of the capillary bed. At the venular end, the junctions consist of low profile ridges on the protoplasmic fracture (PF) face or complimentary grooves on the exoplasmic fracture (EF) face some of which have a sparse number of associated particles. The vascular junctions are similar to those of vessels in rat omentum and mesentery, and resemble "leaky" junctions described in renal proximal convoluted tubular cells. Tight junctions (zonulae occludentes) between type I pneumocytes or between types I and II pneumocytes consist of a band of interconnecting ridges on the PF face and complimentary interconnecting grooves on the EF face. These continuous epithelial junctions have a structure that is typical of tight occluding junctions. Occasionally zonulae occludentes between type I and type II pneumocytes are discontinuous; this may be the result of cell translocation as pneumocytes are shed into the alveolus. Intravascular perfusion fixation at high pressure (140 cm H2O) had no discernible effect on the structure of endothelial or epithelial junctions. The appearance in our study of freeze-fractured pulmonary endothelial and epithelial junctions reveals clearly the physical basis for the results of ultrastructural tracer and physiological studies which have suggested that it is the alveolar epithelium rather than the endothelium that is the chief permeability barrier to small, water-soluble molecules.

Animals↗
PubMed2000

Assembly of intercellular junctions in epithelial cell monolayers following exposure to cryoprotectants.

We investigated the effects of cryoprotectants (glycerol, propane-1, 2-diol, dimethyl sulfoxide) on the ability of epithelial cells to assemble intercellular junctions. Madin-Darby canine kidney cells (MDCK, type II) were grown in S-MEM containing only 5 micromol/L Ca(2+) to allow attachment of cells to the growth surface but not the development of the junctional complex. In a first set of experiments, cells were exposed to 10% v/v cryoprotectant at room temperature for 30 min. After removal of the cryoprotectant, [Ca(2+)] was increased to 1.8 mmol/L (Ca-switch) and the assembly of junctions was followed immunocytochemically and by monitoring transepithelial resistance (TER). In a second set of experiments, the development of junctions was followed in the presence of 1% cryoprotectant. Addition and removal of 10% cryoprotectant had little effect on the assembly of junctions following the Ca-switch, with TER peaking >300 ohm cm(2) after 24 h. Immunocytochemical staining showed recruitment to cell borders of components of tight junctions, adherens junctions, and desmosomes and the presence of a distinct circumferential bundle of actin filaments. In the presence of 1% cryoprotectant, there was a lag of more than 20 h before TER began to rise. There was then a progressive rise in TER in all three cryoprotectant groups, indicating junction assembly, albeit at a lower rate than that in the absence of cryoprotectant. These results suggest that exposure to cryoprotectants per se will not inhibit cellular repair mechanisms aimed at restoring the integrity of epithelial cell layers, but incomplete removal of cryoprotectant may delay repair.

Actin Cytoskeleton↗
PubMed1987

Immunolocalization of MP70 in lens fiber 16-17-nm intercellular junctions.

Thin section electron microscopy reveals two different types of membrane interactions between the fiber cells of bovine lens. Monoclonal antibodies against lens membrane protein MP70 (Kistler et al., 1985, J. Cell Biol., 101:28-35) bound exclusively to the 16-17-nm intercellular junctions. MP70 localization was most dramatic in the lens outer cortex and strongly reduced deeper in the lens. In contrast, the 12-nm double membrane structures and single membranes were consistently unlabeled. In freeze-fracture replicas with adherent cortical fiber membranes, MP70 was immunolocalized in the junctional plaques which closely resemble the gap junctions in other tissues. MP70 is thus likely to be associated with intercellular communication in the lens.

Animals↗
PubMed1994

Expression of cell adhesion molecules and connexins in gap junctional intercellular communication deficient human mesothelioma tumour cell lines and communication competent primary mesothelial cells.

Gap junctional intercellular communication (GJIC) has been reported to be markedly reduced in human mesothelioma tumour cell lines compared with primary mesothelial cells. Immunofluorescence stainings have shown that the gap junction protein connexin43 (Cx43) is expressed in both malignant and normal mesothelial cells. In this study the mRNA expression of Cx43 and three different connexins--Cx37, Cx40 and Cx45, which are highly expressed in lung tissue--was investigated in eight human mesothelioma cell lines, and in human primary mesothelial cells from several donors. The expression of the intercellular adhesion molecules A-CAM (N-cadherin) and L-CAM (E-cadherin) was studied at the protein level. No mRNA expression of Cx37, Cx40 or Cx45 in either mesothelioma tumour cells or the primary mesothelial cells was detected. Cx43 was expressed at both the mRNA and the protein level, in seven out of eight mesothelioma cell lines, as well as in all the primary mesothelial cell cultures. The well as in all the primary mesothelial cell cultures. The intercellular adhesion molecule A-CAM was expressed at the cell-cell borders in six out of seven mesothelioma cell lines, as well as in normal mesothelial cells. No expression of L-CAM was observed in these cells. The results suggest that Cx43 and A-CAM are the major proteins in gap and adherens junctions respectively in human mesothelial cells. Most mesothelioma tumour cell lines with markedly reduced GJIC still express both Cx43 and A-CAM. Only one of our mesothelioma tumour cell lines severely deficient in GJIC lacks both the gap junction protein Cx43 and the cell adhesion molecule A-CAM.

Cell Adhesion Molecules↗
PubMed2000

Biosynthesis and structural composition of gap junction intercellular membrane channels.

Gap junction channels assemble as dodecameric complexes, in which a hexameric connexon (hemichannel) in one plasma membrane docks end-to-end with a connexon in the membrane of a closely apposed cell to provide direct cell-to-cell communication. Synthesis, assembly, and trafficking of the gap junction channel subunit proteins referred to as connexins, largely appear to follow the general secretory pathway for membrane proteins. The connexin subunits can assemble into homo-, as well as distinct hetero-oligomeric connexons. Assembly appears to be based on specific signals located within the connexin polypeptides. Plaque formation by the clustering of gap junction channels in the plane of the membrane, as well as channel degradation are poorly understood processes that are topics of current research. Recently, we tagged connexins with the autofluorescent reporter green fluorescent protein (GFP), and its cyan (CFP), and yellow (YFP) color variants and combined this reporter technology with single, and dual-color, high resolution deconvolution microscopy, computational volume rendering, and time-lapse microscopy to examine the detailed organization, structural composition, and dynamics of gap junctions in live cells. This technology provided for the first time a realistic, three-dimensional impression of gap junctions as they appear in the plasma membranes of adjoining cells, and revealed an excitingly detailed structural organization of gap junctions never seen before in live cells. Here, I summarize recent progress in areas encompassing the synthesis, assembly and structural composition of gap junctions with a special emphasis on the recent results we obtained using cell-free translation/ membrane-protein translocation, and autofluorescent reporters in combination with live-cell deconvolution microscopy.

Animals↗
PubMed2005

Doxorubicin induces EGF receptor-dependent downregulation of gap junctional intercellular communication in rat liver epithelial cells.

Exposure of rat liver epithelial cells to doxorubicin, an anthraquinone derivative widely employed in cancer chemotherapy, led to a dose-dependent decrease in gap junctional intercellular communication (GJC). Gap junctions are clusters of inter-cellular channels consisting of connexins, the major connexin in the cells used being connexin-43 (Cx43). Doxorubicin-induced loss of GJC was mediated by activation of extracellular signal-regulated kinase (ERK)-1 and ERK-2, as demonstrated using inhibitors of ERK activation. Furthermore, activation of the epidermal growth factor (EGF) receptor by doxorubicin was responsible for ERK activation and the subsequent attenuation of GJC. Inhibition of GJC, however, was not by direct phosphorylation of Cx43 by ERK-1/2, whereas menadione, a 1,4-naphthoquinone derivative that was previously demonstrated to activate the same EGF receptor-dependent pathway as doxorubicin, resulting in downregulation of GJC, caused strong phos-phorylation of Cx43 at serines 279 and 282. Thus, ERK-dependent downregulation of GJC upon exposure to quinones may occur both by direct phosphorylation of Cx43 and in a phosphorylation-independent manner.

Animals↗
PubMed1993

Ultrastructural study of rabbit buccal epithelial cells and intercellular junction by scanning and transmission electron microscopy.

We observed by scanning and transmission electron microscopy the ultrastructure on the upper and lower surfaces of buccal epithelial superficial layer cells and the arrangement of intercellular junction apparatuses. In the superficial layer cells of the rabbit buccal epithelium, microvillus-like processes were observed on the lower surface and microridges on the upper surface. The distal portion of the microvillus-like process on the lower cell surface formed a wedge-like structure. At the intermicroridge areas on the upper cell surface, wedge-like depressions were observed. These depressions were interdigitated with the wedge-like structures of the microvillus-like processes. From the observation of the serial ultrathin sections, most interdigitation sites have two demosomes per microvillus-like process (89.5%). The desmosomes were located in the distal portion of the microvillus-like processes (99.3%). The wedge-like structures of the microvillus-like processes and wedge-like depressions on the inter-microridge areas seem to increase the junctional surface and enhance cell cohesion against external forces from various directions.

Animals↗
PubMed1977

Ultrastructural changes of intercellular junctions in rat ascites hepatoma cells with calcium depletion.

To analyse the effect of ethylenediamine tetraacetate (EDTA) on tumour cell adhesiveness, fine structure of intercellular junctions of rat ascites hepatoma cells AH136B and AH7974 (both forming cell islands in vivo) was first compared. The close contact of the apical portion of both cell islands was composed of tight junctions with a narrow gap. The close contact of the inner portion of AH136B cell islands was largely by simple apposition, while that of AH7974 cell islands had many intermediate junctions and desmosomes. Treatment with EDTA (2 mM) induced morphological alteration of simple apposition, intermediate junctions and desmosomes, but tight junctions remained intact. The effect of EDTA on such junctional complexes seemed to be partially reversible on readministration of Ca ions. Changes in desmosomes, as confirmed on AH7974 cells, were initiated by disappearance of the central disc of electron-dense materials, followed by marked opening of intercellular space and disappearance of endoplasmic laminar plaque. These results suggest that Ca ions may be concerned with maintaining the integrity of junctional complexes other than tight junctions.

Animals↗