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At least 919 records · Page 51Linked to original sources
PubMed1990

Infection of rat liver epithelial cells with v-Ha-ras: correlation between oncogene expression, gap junctional communication, and tumorigenicity.

The role of v-Ha-ras oncogene in tumorigenesis in an in vitro/in vivo model system was studied by investigating the expression of the Ha-ras gene, gap junctional intercellular communication, and tumorigenicity as endpoints. Infection of a Fischer 344 rat liver epithelial cell line (WB 344) with a retrovirus containing the v-Ha-ras oncogene resulted in altered cell morphology and decreased contact sensitivity. Gap junctional intercellular communication in v-Ha-ras infected WB cells (WBHa-ras), assessed by fluorescence redistribution after photobleaching (FRAP), microinjection/dye transfer, and scrape-loading/dye transfer techniques, was markedly decreased compared with the level in control WB cells. Injection of 10(7) WBHa-ras cells into the portal vein of male F344 rats caused multiple focal hepatic lesions within 1 and 2 wk, merging to large invading tumors after 3 and 4 wk. Examination of the methylation pattern of the Ha-ras gene in WBHa-ras and control WB cells showed that the infected Ha-ras gene was relatively hypomethylated in comparison to the normal cellular Ha-ras gene, indicating a greater potential for expression. There was an increased level of Ha-ras mRNA in hepatomas as compared with both adjacent nontumor liver tissue and liver tissue obtained from normal animals. Three cell lines derived from three different primary hepatic tumors induced by an injection of WBHa-ras cells in a F344 rat displayed similar growth characteristics, levels of gap junctional communication, and methylation patterns as the original WBHa-ras cells. The results of these studies have established a strong positive correlation between expression of the Ha-ras oncogene, reduced gap junctional intercellular communication, decreased contact sensitivity, and tumorigenicity of the v-Ha-ras-infected rat liver epithelial cells.

Animals↗
PubMed1991

Aberrant expression and function of gap junctions during carcinogenesis.

Gap junctional intercellular communication plays a key role in the maintenance of homeostasis in multicellular organisms. Reflecting deranged homeostasis in cancer cells, most transformed or cancerous cells show aberrant gap junctional intercellular communication; they have decreased junctional communication between each other and/or with surrounding normal cells. Studies with in vitro cell transformation and animal carcinogenesis models suggest an involvement of blocked intercellular communication in later stages of carcinogenesis. Analysis of expression of gap junction proteins (connexins) and corresponding mRNA indicates that a number of regulation sites are involved in aberrant function of gap junctions during carcinogenesis. Suppression of transformed phenotypes is often seen when transformed cells are physically in contact with their normal counterparts. Some studies suggest that gap junctional intercellular communication is involved in such tumor suppression.

3T3 Cells↗
PubMed2004

Intercellular Adhesive Structures Between Stellate Cells - An Analysis in Cultured Human Hepatic Stellate Cells.

To investigate whether or not hepatic stellate cells can form intercellular junctions with each other, we cultured human stellate cells (LI90) on different kinds of substrata. Intercellular junctions were detected between these cultured stellate cells by transmission electron microscopy (TEM). The molecular components of the intercellular adhesive structures were identified by immunofluorescence microscopy. Immunofluorescence for cadherin and catenins was detected at the adhesion sites between the cultured stellate cells. Thus, the intercellular junctions were indicated to be adherens junctions at the molecular level. The junctions developed in the cultured stellate cells irrespective of the type of substratum. These data suggest that the junctional formation between the stellate cells occurs in vivo as well as in vitro.

Journal Article↗
PubMed1988

Cortical bone repair. The relationship of the lacunar-canalicular system and intercellular gap junctions to the repair process.

Repair of cortical bone was studied in 2.4-millimeter-diameter mid-diaphyseal femoral and tibial defects in young New Zealand White rabbits using light microscopy, transmission electron microscopy, and histomorphometry. The initial source of repair tissue is the marrow. Vessels grow into the defect, accompanied by undifferentiated mesenchymal cells. Woven bone is synthesized initially at the periphery of the defect on pre-existing cortex. Differentiating mesenchymal osteoblasts surround themselves with osteoid in a woven conformation. Once a scaffold has formed, surface osteoblasts align themselves in a regular array on the woven matrix surface and synthesize osteoid in a lamellar conformation. The long axes of the repair vessels, lamellae, and osteocyte lacunae are perpendicular to the long axis of the bone. Polarized-light microscopy showed maintenance of this pattern at six, eight, and twelve weeks, even when the defect was filled with lamellar bone. Remodeling is performed slowly by osteoclast cutting cones over a period of several months. The lacunar-canalicular system is clearly demonstrated in plastic-embedded, toluidine blue-stained sections. A canaliculus passes into or away from a lacuna every 1.9 micrometers over the entire osteocyte perimeter. Undifferentiated mesenchymal cells have no processes, as seen by transmission electron microscopy, but soon sprout a florid array of processes as differentiation to early mesenchymal osteoblasts proceeds. Osteoblast and osteocyte cell processes are packed with intermediate filaments that are continuous with those in the cell bodies. Intercellular gap junctions are seen between surface osteoblasts, between osteoblasts and underlying osteocytes, and between osteocyte cell processes in the canaliculi.

Animals↗
PubMed1995

Junctions between early developing osteoblasts of rat calvaria as revealed by freeze-fracture and ultrathin section electron microscopy.

Although intercellular junctions have been described between mature lamellar bone cells, little has been known about junctions between osteoblasts in early developing bone. We therefore conducted a freeze-fracture and ultrathin section study on developing calvaria of rat embryos aged 17-19 days to determine what types of intercellular junctions appear between osteoblasts in early osteogenesis. We observed that three main types of junctional structures, i.e., adherens of the macular type, gap, and focal tight junctions, coexist between osteoblasts in early developing bone. Their possible involvement in early morphogenetic events is discussed. Tight junctions are considered to be involved in compartmentalization of the early matrix and final polarization of osteoblasts.

Animals↗
PubMed1976

Spherical microparticles in human myocardium: an ultrastructural study.

Clusters of spherical microparticles (SMP) that averaged 500 A in diameter and were composed of dense cores surrounded by single trilaminar membranes were found in operatively obtained myocardial biopsies from 29 of 70 patients with various types of heart diseases including: left atrial myocardium (14 patients) and right atrial myocardium (four patients) of 14 patients with mitral valvular disease; left ventricular myocardium of three of 16 patients with aortic valvular disease, three of 16 patients with hypertrophic cardiomyopathy, and two of four patients with combined mitral and aortic valvular disease; and crista supraventricularis muscle of seven of 20 patients with congenital heart diseases associated with muscular obstruction to right ventricular outflow. SMP were consistently associated with interstitial fibrosis and with degeneration of the muscle cells. SMP occurred along the outer surfaces on the sides and free ends of muscle cells in areas of fibrosis, in the widened spaces between membranes of partially dissociated intercellular junctions, and within cytoplasmic vesicles considered to be phagocytic. SMP frequently were joined together by minute nexuses that were structurally identical with those forming parts of intercellular junctions of muscle cells. Evidence is presented to show that SMP occur commonly in tissues other than myocardium. It is concluded that SMP form in the heart as part of a process that mediates the remodeling of cellular surfaces, especially those of intercellular junctions undergoing dissociation.

Cardiomegaly↗
PubMed1977

Exocrine pancreas under experimental conditions. III. Membrane and cell junctions in isolated acinar cells.

The ultrastructure of the cell membrane and intercellular junctions was studied after isolation of exocrine pancreatic cells by tryptic digestion and mechanical treatment. The number and distribution of membrane associated particles does not change significantly when acinar cells in situ are compared to those after the isolation procedure. However, intercellular junctions undergo distinct alterations. Gap junctions in normal pancreatic cells are macular in shape and localized at the lateral parts of the cell membrane. In isolated acinar cells gap junctions are irregularly shaped, more extended, and frequently associated with tight junctions. Tight junctions form belt-like structures which are found to persist after isolation but subsequently become elongated and interrupted. Thus extensive macular areas of tight junctions develop. Further, the strands on the P-face and the grooves on the E-face of freeze-fracture replicas change in array, dissociate, and become loosely packed on large membrane areas. The present investigation shows that the intramembranous proteins of tight and gap junctions are mobile structures within the fluid membrane. The shape of their array is dependent on the form of the intercellular contact zone.

Animals↗
PubMed1987

Cell junctions and the biological behaviour of cancer.

Quantitative and qualitative abnormalities in intercellular junctions have been described in a broad spectrum of human and animal cancers. Current efforts are aimed at exploring the possibility that some of these defects may account for the hallmarks of malignancy, namely tumour invasion and metastasis. This approach is hampered by a paucity of information on the natural history of human cancer. There is evidence from quantitative electron microscopy studies of urinary bladder carcinomas induced by a chemical carcinogen in Fischer rats that decreased intercellular adhesion, mediated in part by intercellular junctions, does not contribute to the invasive potential of tumours. However, it may account for increased cell shedding at the tumour surface. The increased leakiness of malignant epithelium is attributed to defects in occludens junctions. The defects appear to represent a failure to assemble intramembrane fibrils into fully competent occludens junctions, rather than a blockage of fibril synthesis. Gap junctional deficiencies are not an invariant in cancers. Further, gap junctional deficiencies are present in human cervical carcinoma-in-situ. These deficiencies are present many hundreds of cell generations before the development of invasive tumours. This argues against the hypothesis that gap junctions per se contribute to the biological behaviour (i.e. invasion) of malignant tumours.

Animals↗
PubMed2004

Remodeling of myocyte gap junctions in arrhythmogenic right ventricular cardiomyopathy due to a deletion in plakoglobin (Naxos disease).

OBJECTIVES: We tested the hypothesis that defective interactions between adhesion junctions and the cytoskeleton caused by the plakoglobin mutation in Naxos disease lead to remodeling of gap junctions and altered expression of the major gap junction protein, connexin43. BACKGROUND: Naxos disease, a recessive form of arrhythmogenic right ventricular cardiomyopathy, is associated with a high incidence of arrhythmias and sudden cardiac death. Naxos disease is caused by a mutation in plakoglobin, a protein that links cell-cell adhesion molecules to the cytoskeleton. METHODS: Myocardial expression of connexin43 and other intercellular junction proteins was characterized in 4 patients with Naxos disease. Immunohistochemistry was performed in all 4 patients, and immunoblotting and electron microscopy were performed in 1 patient who died in childhood before overt arrhythmogenic right ventricular cardiomyopathy had developed. RESULTS: Connexin43 expression at intercellular junctions was reduced significantly in both right and left ventricles in all patients with Naxos disease. Electron microscopy revealed smaller and fewer gap junctions interconnecting ventricular myocytes. Mutant plakoglobin was expressed but failed to localize normally at intercellular junctions. Localization of N-cadherin, alpha- and beta-catenins, plakophilin-2, desmoplakin-1, and desmocollin-2 at intercalated disks appeared normal. CONCLUSIONS: Remodeling of gap junctions occurs early in Naxos disease, presumably because of abnormal linkage between mechanical junctions and the cytoskeleton. Gap junction remodeling may produce a coupling defect which, combined with the subsequent development of pathologic changes in myocardium, could contribute to a highly arrhythmogenic substrate and enhance the risk of sudden death in Naxos disease.

Adult↗
PubMed1993

Inhibition of chemically induced neoplastic transformation by carotenoids. Mechanistic studies.

In 10T1/2 cells several dietary carotenoids have been shown to be capable of inhibiting carcinogen-induced neoplastic transformation. Their action appears qualitatively similar to the previously documented action of retinoids in this cell system. However, higher concentrations (10-1000-fold) are required. Both types of compound were found to strongly upregulate gap junctional intercellular communication at concentrations which inhibit transformation. Upregulation of gap junctional intercellular communication was caused by the increased expression of connexin 43, a junctional protein. This activity of carotenoids and retinoids is highly correlated with, and has been proposed to be mechanistically linked to, inhibition of transformation in 10T1/2 cells. In this model the gap junction serves as a conduit for growth regulatory signals from normal to initiated cells. These putative signals act to suppress transformation of the initiated cell.

Animals↗
PubMed1991

Evidence for the presence of actin-associated intercellular adhesion junction between interstitial cells of Leydig in the ground squirrel testis.

Interstitial cells of Leydig characteristically occur in clusters around blood vessels. Often these clusters remain intact when interstitial tissues are mechanically separated from other components of the testis. The presence of strong intercellular attachments is most likely one of the factors responsible for maintaining the integrity of Leydig cell clusters. In many tissues, actin associated adhesion junctions commonly provide intercellular attachment. To determine if actin associated adhesion junctions are present between Leydig cells, we have used 1) immunofluorescence to probe for two components that characterize these junctions in other tissues and 2) electron microscopy to examine areas of intercellular contact for evidence of microfilament related adhesion junctions. Isolated clusters of unsectioned cells, which had been fixed and detergent extracted, were probed with the F-actin specific strains rhodamine phalloidin and NBD-phallacidin and with an affinity purified primary antibody raised against human platelet vinculin. In regions of intercellular contact, fluorescence staining with the actin probes was intense and appeared as a solid linear band. Similar regions also stained with the vinculin probe. In double label experiments, actin and vinculin probes were co-distributed at sites of intercellular contact. Zones of intercellular contact, apparently similar to those detected with fluorescence microscopy, were observed at the ultrastructural level. At these sites, subsurface filaments, interpreted by us as actin, formed a dense carpet adjacent to the plasma membrane on each side of the junction. These filaments appeared to be organized into networks rather than discrete bundles.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗
PubMed1997

Remodeling of pineal epithelium in the fetal rat as delineated by immunohistochemistry of laminin and cadherin.

Epithelial remodeling in the rat pineal during fetal development was immunohistochemically analyzed by using antibodies for laminin and cadherin as molecular markers of basal lamina and intercellular junctions, respectively. The proliferation and differentiation of pinealocytes were also investigated in relation to the advance of epithelial remodeling. The pineal anlage of embryonic day 16 is completely covered by basal lamina immunolabeled for laminin. After embryonic day 17, local dissolution of the basal lamina occurs on the epithelial folds, which develop predominantly in the rostral pineal wall. Some pineal cells migrate through these interruptions and form cellular aggregations outside the basal lamina. Cadherin immunostaining reveals focal dissolution of intercellular junctions in epithelial regions protruding into the pineal lumen. Dissolution of the basal lamina and intercellular junctions accompanied by cellular migration into the stromal tissue or into the pineal lumen continues until birth. The distribution of mitotic cells immunolabeled for BrdU is homogeneous throughout the organ during the fetal period, whereas that of differentiating pinealocytes immunoreactive for synaptophysin shows striking regional heterogeneity in close correlation with the remodeling of the pineal epithelium. The migrating cell populations located either outside the basal lamina or inside the pineal lumen are more liable to become synaptophysin-positive than the rest of the epithelium. These results suggest that epithelial remodeling in the fetal pineal is induced, at least in part, by epithelial infolding and that this remodeling promotes the differentiation of pinealocytes.

Animals↗
PubMed2003

Functional analysis of tight junctions.

Epithelial and endothelial cells are joined to each other via a set of intercellular junctions that differ in their morphological appearance, composition, and function. The tight junction or zonula occludens is the intercellular junction that regulates diffusion between cells and therefore allows endothelia and epithelia to form cellular barriers that separate compartments of different composition. This intercellular gate formed by tight junctions is not only highly regulated but is size- and ion-selective and, hence, represents a semipermeable diffusion barrier. In epithelia, tight junctions form a morphological and functional border between the apical and basolateral cell surface domains. They directly contribute to the maintenance of cell surface polarity by forming a fence that prevents apical/basolateral diffusion of lipids in the outer leaflet of the plasma membrane. Here we describe a set of assays that allow the analysis of tight junctions to determine their integrity and functional state.

Cytological Techniques↗
PubMed1986

Three-dimensional reconstruction of endothelial cell gaps in psoriatic vessels and their morphologic identity with gaps produced by the intradermal injection of histamine.

Endothelial cell gaps in psoriatic vessels and histamine-induced gaps in forearm skin of normal controls were reconstructed in 3 dimensions by a computer graphics system. The gaps in psoriatic vessels were present within the cell, at the intercellular junction, or concurrently at both sites. Histamine-induced gaps were found at the intercellular junction or at both intracellular and intercellular locations. The gaps were linear to oval and often contained cytoplasmic processes from one of the endothelial cells, suggesting that gap formation represents a cellular injury rather than a purely physiologic reversible phenomenon.

Adult↗
PubMed1997

Structural maturation of the interface region between the stria vascularis and spiral ligament in the neonatal rat cochlea.

The ultrastructural morphology of the interface region between the stria vascularis (SV) and spiral ligament (SL) was examined in the neonatal rat cochlea via transmission electron microscopy. At postnatal day (PND) 3, morphology of both basal cells and fibrocytes was simple and immature. Only a small number of fibrocytes was observed in the SL. Intercellular junctions between basal cells and fibrocytes, and between adjacent fibrocytes, were few. At PND 7, the number of fibrocytes increased, and more organelles appeared within their cytoplasm. From PND 11 to 14, nuclei of the basal cells appeared to be more spindle-shaped and contained more heterochromatin. The cytoplasm of the fibrocytes was pale, and a greater number of cytoplasmic vesicles and mitochondria emerged. More intercellular junctions were observed between basal cells and fibrocytes at the interface region and between fibrocytes in the SL. By PND 21, the morphology of basal cells and fibrocytes and their intercellular junctions appeared to be adult-like. These morphological observations correlate with previous reports on the functional maturation of the developing rat cochlea.

Animals↗
PubMed2005

Early responses to mechanical load in tendon: role for calcium signaling, gap junctions and intercellular communication.

Tendon and other connective tissue cells are subjected to diverse mechanical loads during daily activities. Thus, fluid flow, strain, shear and combinations of these stimuli activate mechanotransduction pathways that modulate tissue maintenance, repair and pathology. Early mechanotransduction events include calcium (Ca2+) signaling and intercellular communication. These responses are mediated through multiple mechanisms involving stretch-activated channels, voltage-activated channels such as Ca(v)1, purinoceptors, adrenoceptors, ryanodine receptor-mediated Ca2+ release, gap junctions and connexin hemichannels. Calcium, diacylglycerol, inositol (1,4,5)-trisphosphate, nucleotides and nucleosides play intracellular and/or extracellular signaling roles in these pathways. In addition, responses to mechanical loads in tendon cells vary among species, tendon type, anatomic location, loading conditions and other factors. This review includes a synopsis of the immediate responses to mechanical loading in connective tissue cells, particularly tenocytes. These responses involve Ca2+ signaling, gap junctions and intercellular communication.

Animals↗
PubMed1995

Functional properties of human vascular endothelial cadherin (7B4/cadherin-5), an endothelium-specific cadherin.

Human vascular endothelial cadherin (VE-cadherin, 7B4/cadherin-5) is an endothelial-specific cadherin localized at the intercellular junctions. To directly investigate the functional role of this molecule we cloned the full-length cDNA from human endothelial cells and transfected its coding region into Chinese hamster ovary cells. The product of the transfected cDNA had the same molecular weight as the natural VE-cadherin in human endothelial cells, and reacted with several VE-cadherin mouse monoclonal antibodies. Furthermore, it selectively concentrated at intercellular junctions, where it codistributed with alpha-catenin. VE-cadherin conferred adhesive properties to transfected cells. It mediated homophilic, calcium-dependent aggregation and cell-to-cell adhesion. In addition, it decreased intercellular permeability to high-molecular weight molecules and reduced cell migration rate across a wounded area. Thus, VE-cadherin may exert a relevant role in endothelial cell biology through control of the cohesion and organization of the intercellular junctions.

Amino Acid Sequence↗
PubMed1992

Freeze-fracture studies of salivary glands.

Freeze-fracture electron microscopy was employed to study the general morphology, membrane fusion during exocytosis, intercellular junctions in adult and developing salivary glands, and morphological changes of intercellular junctions in secretory stimulation and neoplastic disorders. Intramembranous particles distributed on plasma membranes and organelle-membranes were determined on the basis of particle density per unit. Relationship between distribution and density of particles and functions of membranes and organelles was discussed. Fused membranes took the form of smooth areas of intramembranous particles free on the PF face in the submandibular acinar cells induced by isoproterenol stimulation. The sequence of membrane fusion during secretion was discussed from these freeze-fracture observations. Tight junctions which limited solute diffusion between adjacent cells formed continuous belts around the juxtaluminal region of plasma membrane. Their permeability function was regulated by the number and the geometrical pattern of the tight-junctional strands. The junction appeared late during gestational life, and its development and morphology correlated with the establishment of electrochemical tightness. Similarity in the location and morphology between developmental and neoplastic conditions might indicate reflect the function and degree of cytodifferentiation in salivary gland. Gap junctions were detected as clusters of particles, representing voltage-regulated intercellular channels connecting adjacent cells. The junctions were developmentally regulated, and their size and frequency correlated with the functional activity and with cytodifferentiation in neoplastic disorders. Desmosomes, which appeared as round or elongated clusters of particles, provided the mechanical stability necessary to maintain the organization of acini and ducts.

Animals↗