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Results for “Intercellular Junctions”

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At least 19 recordsLinked to original sources

PubMed1988

An electron microscope study of the development of the exocrine and endocrine pancreas with special reference to intercellular junctions.

Intercellular junctions in pancreatic acinar, duct and endocrine cells were studied by thin section and freeze-fracture methods in developing rats and mice. Undifferentiated cells were joined by the zonula occludens and isolated fragments of tight junctional strands. Small gap junctions were either occasionally associated with tight junctional strands or appeared independent of them. During the morphological differentiation of acinar cells, strands of the zonula occludens developed to form a complicated meshwork while gap junctions rapidly increased in size. Duct cells were joined by the less-developed zonula occludens but gap junctions were rarely seen. In the neonate, intercellular junctions were similar to those in adult acini and intercalated ducts. Endocrine cells were joined by maculae occludentes and small gap junctions. During late prenatal days, the macula occludens increased in size and gap junctions in number. Sometimes tight junctional strands disappeared to leave membrane elevations, some of which were associated with small gap junctions. Maculae occludentes on endocrine cells were gradually fragmentized and diminished during postnatal development. They were completely lost in the rat. These results suggest that intercellular junctions play important roles in pancreatic development. In particular, the transient development of maculae occludentes is associated with endocrine cell development, and intercellular communication mediated by gap junctions may be important for the differentiation of acinar and endocrine cells.

Animals↗

PubMedDate not supplied

Birbeck granules or Birbeck junctions? Intercellular "zipperlike" lattice junctions in eosinophilic granuloma of bone.

Three cases of eosinophilic granuloma of bone exhibited intercellular attachments between histiocytes, with a pentalaminar structure identical to that seen in nearby intracellular Birbeck granules (BG). It is proposed that the term "lattice junction" be coined to describe this organelle, which seems to be expressed only by cells of monocytic-histiocytic lineage. While this finding confirms the ability of the surface membrane to form such structures, it does not necessarily preclude other intracytoplasmic sites of origin for some BG. The previously suggested role of BG in membrane storage and regulation is reiterated as a supportable model for their function.

Adolescent↗

PubMed1990

Comparative effects of phenobarbital, DDT, and lindane on mouse hepatocyte gap junctional intercellular communication.

Gap junctional intercellular communication appears to be important in the regulation of cellular homeostasis, differentiated cell functions, and growth control in adult tissues. Interruption of intercellular communication by chemical compounds has been shown to be a sublethal response to a number of tumor promoters. The mechanism by which tumor promoters inhibit intercellular communication remains unresolved. In the present study the kinetics of inhibition of mouse hepatocyte gap junctional intercellular communication (measured by dye coupling) by three well-established hepatic tumor promoters [phenobarbital, 1,1-bis(4-chlorophenyl)-2,2,2-trichloroethane (DDT), and gamma-hexachlorocyclohexane (lindane)] are compared. All three compounds inhibited intercellular communication in a time- and dose-dependent manner in both freshly plated and 24-hr-old hepatocyte cultures. Following removal of the tumor promoters from the culture medium, intercellular communication was reestablished within 0.5 hr (phenobarbital) to 1.5 hr (DDT and lindane). Prolonged treatment of hepatocytes for up to 48 hr with the three promoters resulted in the continued inhibition of intercellular communication by lindane and DDT, but the development of refractoriness to phenobarbital-induced inhibition of intercellular communication. Concomitant treatment with combinations of the three promoters showed an additive effect of the compounds on inhibition of intercellular communication. Inhibition of intercellular communication by phenobarbital was prevented by addition of the cytochrome P450 enzyme inhibitor SKF-525A. SKF-525A had no effect on the inhibition of intercellular communication induced by lindane or DDT. Coincubation of the three promoters with the cAMP analog 8-bromo-cAMP prevented the promoter-induced inhibition of intercellular communication.

Animals↗

PubMed1985

Studies on the mechanism of phorbol ester-induced inhibition of intercellular junctional communication.

Intercellular gap-junctional communication was measured using [14C]citrulline incorporation in co-cultures of argininosuccinate lyase-deficient human fibroblasts and argininosuccinate synthetase-deficient Chinese Hamster V79 cells. As previously shown, in this system junctional communication is completely inhibited by the tumor promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). In the absence of extracellular calcium, TPA inhibition was less pronounced. However, synergism with calcium ionophore A23187 could not be demonstrated. Chlorpromazine, trifluoperazine and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester partially antagonised the effect of TPA. No antagonism was demonstrable between calmidazolium and TPA. Treatment of co-cultures with exogenous phospholipase C or 1-oleoyl-2-acetylglycerol (OAG) resulted in communication inhibition, suggesting that protein kinase C activation is involved in the mechanism of phorbol ester-mediated communication inhibition. However co-cultures which had been made refractory to TPA by prolonged exposure to high concentrations remained sensitive to inhibition by phospholipase C and OAG. These results suggest either that diacylglycerol can produce other effects independent of protein kinase C activation, or that refractoriness to phorbol esters is not simply due to a decrease in the amount of protein kinase C.

Animals↗

PubMedDate not supplied

Limitations of the scrape-loading/dye transfer technique to quantify inhibition of gap junctional intercellular communication.

Gap junctional intercellular communication (GJIC) is recognized as playing an important role in normal cell proliferation and development. Chemically induced alteration of GJIC has been proposed to be associated with abnormal cellular growth and/or tumor promotion. Several in vitro assays are currently used to determine the effects of chemicals on GJIC between cultured mammalian cells. One of these assays, the scrape-loading dye transfer (SL/DT) technique, is based on monitoring the transfer of the fluorescent dye Lucifer yellow from one cell into adjacent cells via functional gap junctions. The objective of our study was to evaluate and compare various approaches for quantifying results obtained with the SL/DT technique. Confluent cultures of either WB rat liver epithelial cells or LC-540 rat leydig cells were exposed to the animal tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), solvent (0.1% ethanol), or culture medium for one hour at 37 degrees C prior to analysis of GJIC. Inhibition of dye transfer was clearly evident following TPA exposure. Quantification of this dye transfer was assessed via four approaches: manually counting the number of labeled cells; measuring the distance of dye travel from the scrape line; quantifying the amount of cellular dye uptake; and determining the distribution of dye away from the scrape line. Our results suggest that while the SL/DT technique can be effectively used as a tool to determine the qualitative presence or absence of GJIC, its use in quantifying changes in GJIC following chemical exposure is limited. Since concentration-dependent responses are critical in chemical testing, application of the SL/DT method should be restricted to a screening assay for qualitatively assessing the presence or absence of GJIC.

Animals↗

PubMed1990

[Morphologic characteristics of intercellular junctions in early embryogenesis of mice].

Dynamics concerning certain intercellular junctions have been followed during the preimplantation period of development in mouse embryos. The morphological analysis of the preimplantational embryos has demonstrated, that at the initial stages of cleavage (2-4 blastomeres) the cells make contacts by means of nonspecific junctions. Specialized intercellular junctions appear at the stage of 8 blastomeres and are presented as dotted tight and gap junctions. When the embryo is developing from the stage of 8 up to the stage of 16 blastomeres, certain connective complexes appear, consisting of dotted or cord-like tight and gap junctions. At the late morula stage, the external blastomeres in the apical part have contacts with each other by means of cingular tight junctions. In this place a connective complex might emerge; it is displayed as a tight junction and one or two gap junctions. At the blastocyst stage desmosomes and adhision zones appear. Between trophectodermal cells a connective complex arises; it is presented in the slice as a tight cingular junction, desmosomes (as a rule two) and an adhision zone. Between cells of the internal cellular mass the intercellular junctions are presented as dotted tight and gap junctions. Cells of the polar trophoectoderm and cells of the internal cellular mass could have contacts by means of gap and dotted tight junctions.

Animals↗

PubMed1990

Inhibition of gap-junctional intercellular communication and enhanced binding of fibronectin-coated latex beads by stimulation of DNA synthesis in quiescent 3T3-L1 cells.

To clarify the modulation of intercellular communication via gap junctions, associated with the growth induction of quiescent 3T3-L1 cells, we investigated the gap-junctional intercellular communication in growth-stimulated cells that were able to bind fibronectin-coated beads. When quiescent 3T3-L1 cells were incubated with fibronectin-coated beads for the first 2 h after the addition of calf serum, 24.0% of the cells bound and phagocytosed beads. Among the cells with bound beads, the percentage of the cells labeled concurrently with bromodeoxyuridine was 63.7% when examined 13 h after the addition of calf serum. Transient reduction of dye-coupling, measured with Lucifer Yellow CH, was observed only in the cells with bound beads 2 h after addition of calf serum, but it was not observed in the cells without bound beads. When the quiescent cells were incubated with fibronectin-coated beads for 2 h from 4-6 h after the addition of calf serum, the percentage of cells with bound beads increased to 53.1%, but the decrease in dye-coupling among the cells with bound beads was slight. These results suggest that the induction of cell growth causes a transient reduction in gap-junctional intercellular communication in 3T3-L1 cells with bound fibronectin-coated beads.

Animals↗

PubMed1987

Restoration of LDL receptor activity in mutant cells by intercellular junctional communication.

Exchange of small molecules between cells through intercellular junctions is a widespread phenomenon implicated in many physiological and developmental processes. This type of intercellular communication can restore the activity of low-density lipoprotein (LDL) receptors in mammalian cells that are deficient in the enzyme UDP-Gal/UDP-GalNAc 4-epimerase. Pure cultures of the 4-epimerase mutant are unable to synthesize normal carbohydrate chains on LDL receptors and many other glycoproteins and therefore do not express LDL receptor activity. When these cells are cocultivated with cells expressing normal 4-epimerase activity, the structure and function of LDL receptors are restored to normal by the transfer of this enzyme's products through intercellular junctions. The formation of functional junctions does not require normal glycosylation of membrane proteins. Because many convenient assays and selections for LDL receptor activity are available, this mutant can provide a powerful new tool for biochemical and genetic studies of intercellular junctional communication.

Animals↗

PubMed1977

Ultrastructure and distribution of intercellular junctions in corneal endothelium.

The intercellular junctions of the corneal endothelium has been studied in rabbit, monkey and human eyes. A union of apposing outer leaflets (tight junction) is usually found near the apical end of the intercellular clefts. However, evidence from lanthanum tracer studies indicates that the tight junctions do not seal the intercellular clefts completely. In addition to tight junctions, the presence of gap junctions or nexuses is demonstrated in all three species studied.

Animals↗

PubMed1975

[Highly permeable intercellular junctions in normal and transformed fibroblast cultures].

Intercellular junctions permeable to ions and fluorescein Na were studied with the aid of intracellular microelectrodes in the cultures of normal and transformed mouse-embryo and hamster-embryo fibroblast-like cells. Normal cells were effectively coupled by the highly permeable junctions. In cultures of 7 types of transformed cells, 3 types of coupling were detected: effective, decreased, and fully reduced couplings. The degree of uncoupling was not correlated with morphological patterns of malignization and tumorogeneity of transformed cultures. The decrease of permeability of intercellular junctions to ions and small molecules is concluded not to be necessary for malignization.

Animals↗

PubMed1990

Lack of correlation between intercellular junctional communication, p21rasEJ expression, and spontaneous metastatic properties of rat mammary cells after transfection with c-H-rasEJ or neo genes.

The loss of intercellular junctional communication between rat 13762NF mammary carcinoma cells and their spontaneous metastatic potentials from the mammary fat pad show a high degree of correlation. We examined a stable, benign, completely junctionally coupled cell clone (MTC.4) of this system after calcium phosphate-mediated transfection with c-H-rasEJ/pSV2neo and control pSV2neo-containing plasmids. There was a good correlation between the copy numbers of c-H-rasEJ incorporated into MTC.4 cells and their contents of p21rasEJ; however, there was not always a correspondence between spontaneous metastatic potential and copy number of c-H-rasEJ or amount of p21rasEJ. After c-H-rasEJ/pSV2neo transfection, some MTC.4 cells lost intercellular junctional communication and became spontaneously metastatic, although some nonmetastatic transfectants also had low percentages of junctionally coupled cells. One of the control pSV2neo transfectants also became metastatic and lost intercellular junctional coupling, and calcium phosphate treatment itself resulted in increased growth rates at mammary fat pad sites and a marginal increase in incidence of spontaneous metastases, both of which preceded loss of intercellular junctional coupling in some cells. Examination of 12 subclones derived from two cloned transfectants, however, revealed a poor correlation between spontaneous metastatic potential and intercellular junctional coupling. The results suggest that loss of junctional communication between cells is often but not always associated with the progression of cells from benign to metastatic states.

Animals↗

PubMed1989

Potential role of the human Ha-ras oncogene in the inhibition of gap junctional intercellular communication.

The modulation of gap junctional intercellular communication (GJIC) plays an important role during tumor promotion. Several tumor-promoting agents are known to inhibit this form of cellular coupling. In addition, tumor cells and cells expressing certain oncogenic products have been shown to exhibit inhibited or reduced GJIC. The Ha-ras oncogene is expressed in a wide variety of human tumors from different tissues. Its p21 product is a membrane-bound polypeptide, the function of which is not fully characterized. We tested the effects of the expression of the human c-Ha-ras-1 oncogene, derived from the EJ/T4 bladder carcinoma cell line, on the ability of the Chinese hamster V79 cells to conduct gap junctional communication. The junctional competence was studied by two different methods, the scrape-loading/dye transfer technique and the metabolic cooperation assay. The results indicate a strong correlation between the expression of p21 ras protein and the inhibition of gap junctional function. Assuming that reversible inhibition of intercellular communication plays a role during tumor promotion and stable inhibition during the tumor progression phase of carcinogenesis, our data suggest that, while chemical tumor promoters and the ras oncogenes might work by different biochemical mechanisms, they both affect a critical cellular function; namely, GJIC.

Animals↗

PubMed1977

Intercellular junctions in the central nervous system of insects.

The intercellular junctional complexes in the central nervous system (CNS) from a variety of insect species have been examined by thin-sectioning and freeze-fracturing techniques. Of particular concern has been the fine-structural basis of the blood-brain barrier observed to be present in the outer perineurial layer around the avascular insect CNS. The basis of this has been found in the form of tight junctions (zonulae occludentes) present both in sections and in replicas of the perineurium. In the latter, they appear as one or two simple linear ridges, lying parallel to the outer surface, which occasionally display overlapping. The complex geometry of the interdigitating perineurial cells apparently permits such a relatively simple series of ridges to function as a barrier, since tracers are found not to penetrate beyond this level into the underlying nervous tissue. Such evidence is supported by microprobe X-ray analysis of lanthanum-incubated tissues, the perineurium compared with the glia-ensheathed axons showing the presence and absence of lanthanum, respectively. Possible physiological mechanisms that could operate 'in vitro' to maintain the blood-brain barrier are also considered. Other intercellular junctions such as desmosomes, septate junctions and gap junctions are found in the perineurial layer too, the last exhibiting EF particle plaques and PF pits. Glia-glia junctions also occur in some insect species; they include desmosomes, inverted gap junctions and occasional tight junctions. Septate, gap and tight junctions are also found on the membranes of tracheoles penetrating the CNS. Short, ridge-like elaborations and other particle arrays are found on the PF on the axon surfaces and the significance of these structures is discussed.

Animals↗

PubMed1985

Intercellular junctions between human odontoblasts. A freeze-fracture study after demineralization.

Intercellular junctions in the odontoblastic layer have been studied with a freeze-fracture technique. Children's tooth germs were fixed, sliced and demineralized. Samples of the pulpodentinal border were routinely prepared for freeze-fracture. Three kinds of intercellular junctions were detected between human odontoblast cell bodies: gap junctions, desmosomes and tight junctions. Numerous gap junctions are responsible for intercellular communication at different levels of the cell bodies. Focal tight junctions, parallel to the axis of the cell, and desmosomes are sites of cell-to-cell adhesion between lateral plasma membranes. At the distal end of the cell bodies, junctional complexes consist of zonular tight junctions and gap junctions. These zonular tight junctions, never before described between odontoblasts, contribute to the pseudo-epithelial organization of the odontoblastic layer. They constitute a predentin-pulp barrier, the permeability of which must be studied to establish their role in relation to dentin formation.

Adolescent↗

PubMed1992

The role of the cytoskeleton and intercellular junctions in the transcellular membrane protein polarity of bovine aortic endothelial cells in vitro.

This project examines the transcellular membrane protein polarity of bovine aortic endothelial cell (BAEC) monolayers in vitro with respect to the roles that intercellular junctions (as defined by comparing confluent and subconfluent monolayers) and the submembranous cytoskeleton play in controlling this phenomenon. Plasma membrane (PM) proteins obtained from apical (AP) and basolateral (BL) PM domains of confluent BAEC monolayers were isolated using the cationic colloidal silica technique and resolved by two-dimensional gel electrophoresis (2-D PAGE). To facilitate the identification of domain-specific PM proteins, an isoelectric point/molecular weight database of the proteins from AP and BL PM domains was constructed. Domain-specific PM proteins were assessed for their interaction with the cytoskeleton by determining whether they co-isolated with a Triton X-100 detergent-resistant cytoskeletal/extracellular matrix fraction. The maintenance of polarized PM protein segregation by intercellular junctional complexes was determined by comparing AP and BL protein patterns of confluent monolayers with patterns generated by subconfluent monolayers, which lack such junctional structures. Proteins isolated from AP and BL PM domains from both confluent states were immunoblotted with antibodies to angiotensin-converting enzyme (ACE) and collagen receptors (CR). ACE was restricted exclusively to the AP PM domain in the subconfluent condition, even though no apparent cytoskeletal interaction was observed. CRs, found to interact with the cytoskeleton in either confluence state, were predominantly segregated to the BL PM domain regardless of the presence or absence of cell-cell contact. Membrane proteins found by 2-D PAGE to be asymmetrically distributed in the absence of intercellular junctions were assessed for cytoskeletal interaction by their inability to be extracted by Triton X-100 from monolayers in the subconfluent state. Computer cross-referencing of 2-D PAGE peak lists and immunodetection generated from the above fractionation protocols identifies a set of four proteins associated with the cytoskeleton that remain segregated in the proper domain, and five proteins associated with the cytoskeleton that become equally distributed between AP and BL PM domains in the absence of intercellular junctions. Additionally, six proteins not associated with the cytoskeleton remain asymmetrically distributed to the AP domain in the subconfluent state. The data suggest that BAEC monolayers have unknown mechanisms, apart from intercellular junctions expressed at confluency or cytoskeletal binding, for maintaining transcellular PM protein polarity.

Animals↗

PubMedDate not supplied

Intercellular junctions in the differentiating rat otocyst.

Intercellular junctions between cells of the rat otocyst on the 12th day of gestation were studied using lanthanum tracer and freeze-fracture techniques. At the luminal surface, the intercellular space is closed by a series of tight junctions. Gap junctions are also present between cells both within and below the luminal junctional complex. The presence of tight and gap junctions at this early stage in the differentiating otocyst is probably essential for the development of a normally functioning adult ear.

Animals↗

PubMed1987

Scrape-loading and dye transfer. A rapid and simple technique to study gap junctional intercellular communication.

Gap junction-mediated intercellular communication has been recognized in cells from different tissues of various organisms and has been implicated in a variety of cellular functions and dysfunctions. Here we describe a new, direct and rapid technique with which to study this cellular phenomenon. It employs scrape-loading to introduce a low molecular weight (MW) fluorescent dye, Lucifer yellow CH (MW 457.2) into cells in culture and allows the monitoring of its transfer into contiguous cells. In communication-competent cells the dye transmission occurred within minutes after loading. The involvement of membrane junctions in Lucifer yellow transfer was verified by the concurrent loading of a high MW marker dye conjugate, rhodamine dextran (MW 10,000). Once introduced intracellularly the rhodamine dextran is unable to cross the relatively narrow membrane junctions. Chemicals of variable potency known to block junctional communication were tested in Chinese hamster V79 cells and other mammalian cells. The results showed effective blockage of the dye transfer at non-cytotoxic doses. This new technique can be applied to a wide variety of mammalian (including human) cells. In addition, it has the potential to be utilized as a rapid screening assay to detect chemicals that can modulate intercellular communication and to study their mechanism of action.

Animals↗

PubMed1985

Effects of 12-O-tetradecanoylphorbol-13-acetate and retinoids on intercellular junctional communication measured with a citrulline incorporation assay.

Inhibition of intercellular junctional communication by 12-O-tetradecanoylphorbol-13-acetate (TPA) and retinoids was investigated using a citrulline incorporation assay. This new assay uses metabolic co-operation between argininosuccinate lyase-deficient human fibroblasts and arginosuccinate synthetase-deficient cells as a measure of junctional communication. Short-term exposure to TPA resulted in virtually complete inhibition of metabolic co-operation when V79 cells were used as the synthetase-deficient type. When synthetase-deficient human fibroblasts were used, inhibition by TPA was only partial. Exposure to high concentrations of TPA for prolonged periods resulted in partial reversal of communication inhibition and a refractory state in which cells were unresponsive to TPA. Retinoic acid and other retinoids also inhibited metabolic co-operation, but did not cause desensitisation of the type seen with TPA after prolonged exposure. Cultures which had been made refractory to TPA remained sensitive to inhibition by retinoic acid and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, indicating that these latter compounds inhibit junctional communication by a mechanism different from TPA. Simultaneous exposure of cultures to TPA and retinoic acid showed that the inhibitory effects on metabolic co-operation of these compounds were additive. Fluocinolone acetonide did not antagonise the effect of TPA. These results suggest that retinoic acid and fluocinolone acetonide exert their anti-tumor-promoting action by mechanisms which are not mediated by intercellular junctional communication.

Animals↗