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Results for “Intercellular Junctions”

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PubMed1995

Molecular organization and functional regulation of cell to cell junctions in the endothelium.

Intercellular junctions are important structural determinants of endothelial permeability. These organelles are formed by a complex network of transmembrane proteins linked to a well developed plasmalemmal undercoat. One of the typical characteristics of endothelial junctions is their dynamic organization. Endothelial cells are able to rapidly change the architecture of the junctions to allow the passage of plasma constituents and circulating cells. This effect, in most of the cases, is quickly reversible and the endothelium is able to disorganize/reorganize the intercellular junctions within minutes. The mechanisms that regulate the opening and the closure of endothelial junctions are still obscure. It is conceivable that inflammatory agents increase permeability by binding to specific receptors generating intracellular signals which in turn cause cytoskeletal reorganization and opening of interendothelial gaps. Endothelial junctions also control leukocyte extravasation. Once leukocytes have adhered to the endothelium, a coordinated opening of interendothelial clefts occurs. The mechanism by which this takes place is unknown, but it might present characteristics similar to that triggered by soluble mediators.

Animals↗
PubMed1986

A possible phagocytic role for folliculo-stellate cells of anterior pituitary following estrogen withdrawal from primed male rats.

Ultrastructural changes suggesting a phagocytic role for the nongranular folliculo-stellate cells of the anterior pituitary are investigated in estrogen-primed male rats after withdrawal of estrogen. Morphological changes in mammotropes following the removal of a subcutaneous estradiol-containing Silastic implant include the formation of intracellular lipid bodies. These lipid bodies appear to be associated with enhanced estrogen-dependent prolactin secretion in mammotropes. Seven and 24 h after estrogen withdrawal intracellular lipid within mammotropes seems to be released into the intercellular space. Seventy-two h after estrogen withdrawal, lipid droplets are almost entirely cleared from mammotropes while folliculo-stellate cells become packed with lipid globules. Folliculo-stellate cells also undergo dramatic hypertrophy 7 and 24 h after the removal of E2-containing implants. Extensive intercellular junctions including zonulae adhaerentes, desmosomes, and putative gap junctions are formed. Intercellular junctions delineate extravascular channels into which numerous microvilli project. Folliculo-stellate cells appear capable of accumulating many lipid droplets, presumably related to mammotrope metabolism. What appear to be large secondary lysosomes as well as the lipid droplets are observed within folliculo-stellate cells; lipid, therefore, may be degraded through a lysosomal pathway in folliculo-stellate cells.

Animals↗
PubMed2003

Localization of intercellular adherens junction protein p120 catenin during podocyte differentiation.

To reveal the role of cadherin complex in podocyte differentiation, the present study describes the localization of the cadherin complex, including p120 catenin (p120ctn), in the developing and in the aminonucleoside nephrosis (PAN nephrosis) rat kidney, by immunofluorescence microscopy and immunogold electron microscopy. p120ctn and beta-catenin were co-localized at the apical part of lateral cell membranes in presumptive podocytes of the S-shaped body, and their localization shifted to the basal margin of lateral cell membranes in the capillary loop stage. There was no expression of the cadherin complex at the slit diaphragm, the intercellular junction of mature podocytes. After the regression of the podocyte junctional structure in PAN nephrosis, the cadherin complex was not re-expressed. The dynamic changes in the localization of the cadherin complex suggest that the it plays an important role during podocyte differentiation, including the rearrangement of the intercellular junction and the formation of the slit diaphragm.

Adherens Junctions↗
PubMed2003

Mass transport in arteries and the localization of atherosclerosis.

Atherosclerosis is a disease of the large arteries that involves a characteristic accumulation of high-molecular-weight lipoprotein in the arterial wall. This review focuses on the mass transport processes that mediate the focal accumulation of lipid in arteries and places particular emphasis on the role of fluid mechanical forces in modulating mass transport phenomena. In the final analysis, four mass transport mechanisms emerge that may be important in the localization of atherosclerosis: blood phase controlled hypoxia, leaky endothelial junctions, transient intercellular junction remodeling, and convective clearance of the subendothelial intima and media. Further study of these mechanisms may contribute to the development of therapeutic strategies for atherosclerotic diseases.

Animals↗
PubMed1986

Focal tight junctions between mesenchymal cells of fetal dermis.

This freeze fracture study shows the presence of focal tight junctions (maculae occludentes) between the mesenchymal cells in the connective tissue matrix of embryonic and fetal dermis. The overall outline of these unique junctions varies from circular to very angular. The junctional elements are most frequently present in a groove on the E fracture face. The corresponding P fracture face has ridges delineating the junction. These intercellular junctions may provide a means of informational or metabolic coupling between cells, may serve a structural role as scaffolding in the deposition and orientation of extracellular materials, or may be involved in the early stages of angiogenesis.

Connective Tissue↗
PubMed1986

Prostaglandins change cell shape and increase intercellular gap junctions in osteoblasts cultured from rat fetal calvaria.

Mounting experimental evidence indicates that osteoblasts may be cellular intermediaries in the local activation of bone remodeling. To elucidate the role of these cells in activation, we examined the effects of prostaglandins (PGs), known resorption stimulators, on cell shape and intercellular junctional relationships in osteoblasts cultured from rat fetal calvaria. Exposure to PGE2 and PGE1, promoters of bone resorption, rapidly (within 20 min) converted the osteoblasts from a flattened to a stellate shape (shape change), and markedly increased the appearance of intercellular (gap) junctions within 10 min. Both effects were directly related to the prostaglandin concentration, as little as 1 nM being effective. PGE1, but not PGB1, PGF1 alpha, PGD2, and PGF2 alpha, mimicked the substantial effect of PGE2 on shape change. Shape change and gap junction formation appear to arise independently. PTH, an inducer of shape change, did not affect the number of gap junctions appreciably. Colchicine, a microtubule polymerization inhibitor, and trifluoperazine, an inhibitor of calmodulin action, blunted PGE2-mediated shape change but not the effect of PGE2 on gap junctions. Shape change and gap junction formation may be important events in local activation, shape changes in surface osteoblasts serving to expose bone surfaces which are chemotactic for osteoclasts and gap junctions propagating locally initiated activation messages.

Animals↗
PubMed1995

Inhibition of intercellular communication via gap junction in cultured aortic endothelial cells by elevated glucose and phorbol ester.

Gap junctional intercellular communication (GJIC) is important in coordinating the cells in maintaining tissue homeostasis and in regulating signal transmission. We examined the effect of elevated glucose on GJIC activity in cultured bovine aortic endothelial cells. GJIC activity was assessed by quantitating the transfer from cell to cell of directly microinjected fluorescent dye molecules. GJIC was activated in the subconfluent monolayer. In this condition, exposing the cells to elevated glucose (400 mg/dl) for 24 hrs significantly inhibited GJIC activity, as compared with low glucose (100 mg/dl). This inhibition of GJIC activity induced by elevated glucose was mimicked by addition of 12-O-tetradecanoylphorbol-13-acetate and was restored by addition of staurosporin (10(-8)M), a PKC inhibitor. These results suggest that inhibition of GJIC activity induced by elevated glucose probably through activation of PKC may be involved in the vascular endothelial cell dysfunction associated with diabetes.

Alkaloids↗
PubMed2003

Low power millimeter wave irradiation exerts no harmful effect on human keratinocytes in vitro.

Low power millimeter wave (LP-MW) irradiation has been successfully used in clinical practice as an independent and/or supplemental therapy in patients with various diseases. It is still not clear, however, whether exposed skin is directly affected by repeated LP-MW irradiation and whether cells of the epidermis can be activated by the absorbed energy. Keratinocytes, the most numerous component of the epidermis are believed to manifest functional responses to physical stimuli. In this study we analyzed whether LP-MW irradiation modulated the production of chemokines, including RANTES and IP-10 of keratinocytes in vitro. We also investigated whether LP-MW irradiation induces a heat stress reaction in keratinocytes, and stimulates heat shock protein 70 (Hsp70) production. Vital staining of keratinocytes with carboxyfluorescein succinimidyl ester and ethidium bromide was used to analyze the MW effect on the viability of adherent cells. In addition, we studied the effect of LP-MW irradiation on intercellular gap junctional communication in keratinocyte monolayers by Lucifer yellow dye transfer. We found no significant changes in constitutive RANTES and inducible IP-10 production following LP-MW irradiation. LP-MW exposure of keratinocyte monolayers did not alter Hsp70 production, unlike exposure to higher power MWs (HP-MW) or hyperthermia (43 degrees C; 1 h). LP-MW irradiation and hyperthermia did not alter the viability of adherent keratinocytes, while HP-MW irradiation induced cellular damage within the beam area. Finally, we found no alteration in the gap junctional intercellular communication of keratinocytes following LP-MW irradiation, which on the other hand, was significantly increased by hyperthermia. In summary, we detected no harmful effect of LP-MW irradiation on both keratinocyte function and structure in vitro, although these cells were sensitive to higher MW power that developed heat stress reaction and cellular damage. Our results provide further evidence that LP-MW irradiation does not induce evidence of skin inflammation or keratinocyte damage and that its clinical application appears to be safe.

Cell Communication↗
PubMed2002

[Intercellular gap junctions in corporal smooth muscle].

The contractility of corporal smooth muscle plays a critical role in human penile erectile process. Understanding the initiation, maintenance and modulation of corporal smooth muscle tone is a prequisite to improve understanding, diagnosis and treatment of erectile dysfunction. Despite this fact, indentification of both the precise mechanistic basis by which various agents exert their effects on individual corporal smooth muscle cells, moreover, the process by which these signals are spread among the diverse array of parenchymal cells in the paired corporal, remain somewhat of a physiological enigma. Therefore, this article aims at: 1. to review current knowledge of the regulation of corporal smooth muscle tone at the cellular and molecular level; 2. to review various methods used in the study of gap junction channel.

Animals↗
PubMedDate not supplied

Cytodifferentiation and dynamics of intercellular relations during early ontogenesis.

The paper presents ultrastructural aspects related to zygotes and embryo cytodifferentiation of Sus scrofa d., used in the biotechnology of embryo transfer, from the first division of segmentation to the stage of preimplantational blastocyst. Together with the intense cellular proliferations, the morphostructural and functional differentiation of cells takes place. First, the blastomeres are similar from an ultrastructural point of view and do not present intercellular junctions to the advanced stage of morula. Gradually, the polarity of the cellular surface is more evident (microvilli occupy only certain domains of the cellular surface and junctions of intercellular solidarity of desmosomal type occur). Ultrastructural modifications of nuclei, mitochondria and cytoskeleton are noticed. Embryoblastic cells as well as those to form the trophoblast are morphostructurally and positionally differentiated. In the stage of preimplantational blastocyst, the nuclei of some embryoblastic cells have a characteristic form of a callotte or biconcave lens with passages of nuclear material to the cytoplasm.

Animals↗
PubMed1996

Modulation of intercellular communication between smooth muscle cells by growth factors and cytokines.

We recently reported that tumor necrosis factor alpha is able to cause a dose-dependent and persistent reduction in gap junctional intercellular communication between primary human smooth muscle cells. In order to study whether this observed persistent reduction in gap junctional intercellular communication is a unique feature for tumor necrosis factor alpha, the present study focuses on the effects of other growth factors and cytokines on gap junctional intercellular communication. Platelet-derived growth factor AA and BB (PDGF-AA, PDGF-BB), basic fibroblast growth factor (bFGF), interleukin-6 and interferon-gamma were able to modulate gap junctional intercellular communication between primary human smooth muscle cells in vitro. However, our results demonstrate that the magnitude and nature of the observed effects are growth factor- and cytokine-specific. PDGF-AA, PDGF-BB and interleukin-6 caused a transient reduction in gap junctional intercellular communication, while bFGF induced a transient increase in gap junctional intercellular communication. Interferon-gamma was shown to be capable of causing a persistent reduction in gap junctional intercellular communication. In addition, PDGF-AA, PDGF-BB, bFGF, interleukin-6, interferon-gamma and tumor necrosis factor alpha all stimulated smooth muscle cell proliferation. These observations suggest a more complex relationship between modulation of gap junctional intercellular communication and cell proliferation than current hypotheses imply. The implications of the observed effects of growth factors and cytokines on gap junctional intercellular communication between smooth muscle cells in relation to the process of atherosclerosis is discussed.

Arteriosclerosis↗
PubMed1994

Gap junction-mediated intercellular communication in primary cultures of rainbow trout hepatocytes.

Gap junction-mediated intercellular communication was evaluated in primary cultures of rainbow trout hepatocytes by measurement of dye coupling. Donor hepatocytes were microinjected with fluorescent Lucifer yellow CH dye and visualization of dye spread (dye coupling) to adjacent hepatocytes was recorded. A maximum level was reached between 8 and 12 hr which was maintained up to 24 hr. Dye coupling then decreased over the next 48 hr. Cell viability was monitored by the percentage of total LDH released and trypan blue exclusion at each time point. The effect of 12-O-tetradecanoylphorbol-13-acetate (TPA), a known inhibitor of rodent hepatic intercellular communication, on gap junction-mediated intercellular communication was evaluated in 24-hr cultures. A dose-response inhibition was demonstrated with maximum inhibition observed at 3 hr of exposure.

Animals↗
PubMed1978

Structural basis for some permeability properties of the air--blood barrier.

The structural basis for the permeability of the alveolar-capillary membrane to water-soluble solutes rests in part on the structure and function of its intercellular junctions and the pinocytotic vesicles within its cells. Intercellular junctions between endothelial cells of the pulmonary capillary bed differ both in permeability to enzyme tracers and in their structure. As determined by freeze fracture, the junctions in the arteriolar, capillary, and venular portion of the capillary network vary in complexity, and in the number of rows of particles constituting the junction. Because there are few particles associated with the junctions in the venular end of the capillary bed, these are considered to be the most permeable of the three types of vascular junctions. Epithelial junctions, in contrast, are impermeable to all enzyme tracers studied, and they are composed of a continuous, complex network of junctional fibrils. While intercellular junctions form seals of varying 'tightness,' pinocytotic vesicles provide a means for the transport of water-soluble macromolecules across the alveolar-capillary membrane.

Animals↗
PubMed1977

Organization of cell junctions in the peritoneal mesothelium.

Intercellular junctions in the mesothelium of the visceral (mesentery and omentum), and parietal (diaphragm, pre-aortic, and iliac region) peritoneum were examined in rats and mice by using freeze-cleaved preparations. In addition to usual intercellular junctions (cell body junctions), special junctions are found between cell processes and the surface of the neighboring cell (cell process junctions). Cell body junctions are provided with tight junctions and communicating (gap) junctions. The former consist of one to two junctional strands which show a characteristic staggered arrangement, and focal discontinuities. In cell process junctions, the strands form loops or appear as short, free-ending elements; their polymorphism suggests considerable lability, probably in connection with their assembly and disassembly. The existence of free-ending strands indicates that such structures can be used as attachment devices without being concomitantly involved in the formation of occluding zonules. In both types of junctions, the strands can be resolved into bars, approximately 80- 100nm long, frequently provided with terminal enlargements and intercalated particles which occur singly or in small clusters. These particles are morphologically similar to those present in communicating (gap) junctions. The mesothelium is also provided with isolate composite macular junctions. Throughout the mesothelium, the cleavage plane follows the outer contour of junctional strands and particles, suggesting that strand-to-strand interactions in the apposed membranes are weaker than interactions between each strand and underlying cytoplasmic structures. In their general geometry and cleavage characteristics, the mesothelial junctions resemble the junctions found in the venular endothelium.

Animals↗
PubMed2002

Neoplastic reversal of human ovarian carcinoma cells transfected with connexin43.

Gap junctional intercellular communication and expression of gap junction proteins (connexins) are decreased frequently in neoplastic cells including human ovarian carcinoma cells. In order to test the hypothesis that these changes contribute to the neoplastic phenotype of ovarian carcinoma cells, we transfected human ovarian carcinoma SKOV-3 cells with connexin43. Stable, connexin43-expressing transfectants were characterized for cell proliferation in vitro in normal, low-serum, and serum-free culture medium, for tumorigenicity in nude mice, and for sensitivity to adriamycin in vitro. Transfected clones expressed higher levels of connexin43 and gap junctional intercellular communication, reduced proliferation and greater dependence upon serum for growth in vitro, decreased tumor formation, increased sensitivity to adriamycin, and reduced expression of p-glycoprotein. These data suggest that gap junctional intercellular communication and/or connexin43 expression suppresses the neoplastic phenotype of ovarian carcinoma cells and their downregulation is involved in neoplastic transformation of ovarian epithelial cells. The increased sensitivity to adriamycin and elevated expression of p-glycoprotein by the transfected cells also suggest that gap junctional intercellular communication and connexin43 expression are involved in drug sensitivity and might be manipulated to enhance the clinical response.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Occludin and the functions of tight junctions.

The tight junction or zonula occludens is the most apical structure of the epithelial junctional complex. Tight junctions from semipermeable intercellular diffusion barriers that control paracellular diffusion in a regulated manner. This intercellular junction also acts as an intramembrane fence that prevents the intermixing of apical and basolateral lipids in the exocytoplasmic leaflet of the plasma membrane. Moreover, evidence suggests that tight junction components participate in the regulation of cell growth and differentiation. Occludin was the first identified transmembrane protein of this intercellular junction and received much attention since its molecular characterization. This review discusses experiments that were done with occludin and how they influenced our current thinking of the molecular functioning of tight junctions.

Animals↗
PubMed1986

Influence of lipids on gap-junction-mediated intercellular communication between Chinese hamster cells in vitro.

The influence of lipids on gap-junction-mediated intercellular communication (i.e., metabolic cooperation) between Chinese hamster V79 cells was investigated. Unsaturated free fatty acids (oleate, linoleate, linolenate, palmitoleate, myristoleate, and arachidonate) inhibited metabolic cooperation between 6-thioguanine-resistant, hypoxanthine guanine phosphoribosyltransferase-deficient and 6-thioguanine-sensitive, hypoxanthine guanine phosphoribosyltransferase-proficient V79 cells. Saturated fatty acids (stearate, palmitate, myristate, and arachidate) had no effect. Further characterization of the effects of fatty acids on metabolic cooperation is summarized as follows: a relationship between the degree of unsaturation and the ability of unsaturated fatty acids to inhibit metabolic cooperation could not be established (i.e., inhibition of metabolic cooperation by 18:1 greater than 18:2 = 18:3); longer carbon chain monounsaturated fatty acids are more effective in inhibiting metabolic cooperation (i.e., inhibition of metabolic cooperation by 18:1 greater than 16:1 greater than or equal to 14:1); geometric isomerism is of some importance in determining the efficacy of monounsaturated fatty acids to inhibit metabolic cooperation (i.e., inhibition of metabolic cooperation by cis 18:1 greater than trans 18:1 and cis 16:1 greater than trans 16:1); and the position of the double bond(s) is relatively unimportant (i.e., inhibition of metabolic cooperation by 18:3 = gamma 18:3). Unsaturated diacylglycerol compounds (diolein, dilinolein, and 1-oleoyl-2-acetyl glycerol) inhibit metabolic cooperation; a saturated diacylglycerol compound (distearin) had no effect. The position of the unsaturated fatty acid groups is not of importance in the inhibition of metabolic cooperation by diacylglycerols containing unsaturated fatty acid moieties (i.e., 1,2-diolein and 1,3-diolein are equally efficacious in inhibiting metabolic cooperation; relative inhibition of metabolic cooperation by 18:1 greater than 1-oleoyl-2-acetyl glycerol greater than 1,2-diolein). Alterations of membrane biophysical properties and protein kinase C involvement are discussed as possible mechanisms involved in the inhibition of metabolic cooperation by unsaturated lipid.

Animals↗
PubMed1996

Gap junctions mediate intercellular calcium signalling in cultured articular chondrocytes.

Gap junction-mediated intercellular communication has been implicated in a variety of cellular functions. Among these, signal transduction can be coordinated among several cells due to gap junctional permeability to intracellular second messengers. Chondrocytes from articular cartilage in primary culture respond to extracellular ATP by rhythmically increasing their cytosolic Ca2+ concentration. Digital imaging fluorescence microscopy of Fura-2 loaded cells was used to monitor Ca2+ in confluent and semi-confluent cell layers. Under these conditions, Ca2+ spikes propagate from cell to cell giving rise to intercellular Ca2+ waves. The functional expression of gap junctions was assessed, in confluent chondrocyte cultures, by the intercellular transfer of Lucifer yellow dye in scrape-loading experiments. Intercellular dye transfer was blocked by the gap junction inhibitor 18 alpha-glycyrrhetinic acid. In imaging experiments, the inhibitor caused the loss of synchrony of ATP-induced Ca2+ oscillations, and blocked the intercellular Ca2+ propagation induced by mechanical stimulation of a single cell in a monolayer. It is concluded that gap junctions mediate intercellular signal transduction in cartilage cells and may provide a mechanism for co-ordinating their metabolic activity.

Adenosine Triphosphate↗