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PubMed1993

Monoclonal antibody 7H6 reacts with a novel tight junction-associated protein distinct from ZO-1, cingulin and ZO-2.

The tight junction is an essential element of the intercellular junctional complex; yet its protein composition is not fully understood. At present, only three proteins, ZO-1 (Stevenson, B. R., J. D. Siliciano, M. S. Mooseker, and D. A. Goodenough. 1986. J. Cell Biol. 103:755-766), cingulin (Citi, S., H. Sabanay, R. Jakes, B. Geiger, and J. Kendrick-Jones. 1988. Nature (Lond.). 333:272-275) and ZO-2 (Gumbiner, B., T. Lowenkopf, and D. Apatira. 1991. Proc. Natl. Acad. Sci. USA. 88:3460-3464) are known to be associated with the tight junction. We have generated a monoclonal antibody (7H6) against a bile canaliculus-rich membrane fraction prepared from rat liver. This 7H6 antigen was preferentially localized by immunofluorescence at the junctional complex regions of hepatocytes and other epithelia, and 7H6-affiliated gold particles were shown electron microscopically to localize at the periphery of tight junctions. Immunoblot analysis of a bile canaliculus-rich fraction of rat liver using 7H6, anti-ZO-1 antibody (R26.4C), and anti-cingulin antibody revealed that 7H6 reacted selectively with a 155-kD protein, whereas R26.4C reacted only with a 225-kD protein. Anti-cingulin antibody reacted solely with 140 and 108-kD proteins, indicating that the protein recognized by 7H6 is immunologically different from ZO-1 and cingulin. Immunoprecipitation of detergent extracts obtained from metabolically labeled MDCK cells with R26.4C coprecipitated a 160-kD protein, which corresponds to ZO-2, with ZO-1. However, 7H6 did not react with the 160-kD protein. These results strongly suggest that the 7H6 antibody recognizes a novel tight junction-associated protein different from ZO-1, cingulin and ZO-2.

Animals↗
PubMed1980

Endothelial proliferation and atherogenesis in rabbits with moderate hypercholesterolemia.

The formation and growth of atherosclerotic lesions in experimental hypercholesterolemia has been attributed to endothelial injury. Many injured endothelial cells have been observed in the periphery of the lesions, but few in the central parts. In the present study, we have investigated the distribution of endothelial cells, leucocytes, and smooth muscle cells on the surface of the lesions, as well as the regeneration of the surface cell layer, on dietary induced experimental atherosclerotic lesions. In central areas of the lesions, flat cells with Weibel-Palade bodies and intercellular junctions characteristic of endothelium, were observed on the surface. In peripheral areas of the lesions, surface cells were more bulging and contained many free ribosomes and short cisternae of endoplasmic reticulum, suggesting that these cells were more primitive. Weibel-Palade bodies and typical intercellular junctions suggested that many of the cells should be regarded as endothelial cells. ANAE- positive monocytes were also frequent in these areas. The incorporation of 3H-thymidine was considerably larger over the lesions than in the surrounding normal tissue, suggesting a regeneration of the endothelial cell layer from cells on the lesions. Still regression does not occur after re-endothelialization in dietary induced atherosclerosis. This contrasts with the development of lesions induced by mechanical injury, and may be of importance for understanding the role of hypercholesterolemia in atherogenesis.

Animals↗
PubMed1988

A reassessment of "chordoid sarcoma". Ultrastructural and immunohistochemical comparison with chordoma and skeletal myxoid chondrosarcoma.

The relationship of "chordoid sarcoma" (CS) to chordoma and myxoid chondrosarcoma has been debated for several years. In order to reassess this issue, we studied 5 CS, 5 chordomas, and 3 skeletal myxoid chondrosarcomas ultrastructurally and immunohistochemically. By electron microscopy, CS demonstrated smooth cellular outlines, macular intercellular junctions, and cytoplasmic inclusions of matrix-like material. Chordomas displayed a closely similar fine structural appearance, but in addition contained small, membrane-bound, glycogen-containing inclusions. Skeletal myxoid chondrosarcomas resembled CS, except that the former lesions had spiculated cell membranes and lacked intercellular junctions. Immunohistochemically, all CS cases expressed vimentin and lacked cytokeratin (CK). Leu 7 and S100 protein were seen in four cases each of CS, and three of these tumors demonstrated diffuse or focal reactivity for epithelial membrane antigen (EMA). Similar phenotypic features were seen in chordomas, except that all of them stained diffusely for CK, as well as EMA. Skeletal myxoid chondrosarcomas expressed vimentin, S100, and Leu 7 uniformly, but were devoid of epithelial markers. In aggregate, these data support the classification of "chordoid sarcoma" as a form of chondrosarcoma, but reveal that it may exhibit an "epithelial" antigen in some cases.

Adult↗
PubMed1979

[Early observations of pancreatic ultrastructure during hemorrhagic necrosis in the rat with closed duodenal pouch].

Many problems are still unanswered in the pathogenesis of acute clinical and experimental pancreatic necrosis. A new technique which can be performed in the rat seems a suitable model for reflux pancreatic necrosis without artificial pressure changes in the ductal system. A closed duodenal loop is obtained with ligation proximal and distal to Vater's ampulla and a gastroenteroanastomosis is associated to avoid intestinal obstruction. All the rats die with hemorrhagic pancreatic necrosis in 36 hours. After 12 hours from the operation ductal and acinar lumina are enlarged. In the centroacinar and intercalated duct cells some lysosomes and mitochondria with clear matrix and reduced cristae are detected. Intercellular junctions in ducts and acini have normal morphology. In the basal cytoplasm of acinar cells some prominent autophagic vacuoles are detectable. After 24 hours in the acinar cells autophagic vacuoles are greatly increased and basal cytoplasmic degeneration often occurs, with plasmalemma and basal lamina interruptions. Intercellular junctions are apparently unaffected until cell necrosis sets in. In blood capillaries endothelial cells are swollen, fibrin thrombosis, hemorrhage and leucocyte infiltration are often detectable. As lysosomal activity occurs also in different kinds of experimental pancreatic necrosis, it could be a common pathogenetic factor, responsible for hydrolytic enzyme activation and for vascular damage in the early stages of hemorrhagic pancreatic necrosis.

Animals↗
PubMed1997

Localized deposition of M-cadherin in the glomeruli of the granular layer during the postnatal development of mouse cerebellum.

M-cadherin is a Ca2+-dependent cell adhesion molecule of the cadherin family, initially localized at the areas of contact between myotubes during myogenesis, but also detected in the peripheral nerve and at the adult neuromuscular junction. In this study, searching for the expression of M-cadherin in the adult mouse brain, we observed a restricted expression of M-cadherin in one of the three layers of the cerebellar cortex: the granular layer. M-cadherin was accumulated in structures rich in synapses and other intercellular junctions where mossy fibers connect granule cell dendrites, the glomeruli. This molecule was not expressed in the cerebellum during the first steps of postnatal cerebellar neurogenesis: granule cell proliferation and migration and Purkinje cell alignment. M-cadherin expression was first detected at postnatal day (P) 11, after the establishment of the synaptic connections between mossy fibers and granule cell dendrites. It then accumulated in glomeruli during their phase of maturation which is characterized by the formation of puncta adherentia between granule cell dendrites. M-cadherin was undetectable in the cerebella of the weaver and staggerer mutants, lacking granule cells, and therefore mature glomeruli and puncta adherentia. Furthermore, other components classically associated with intercellular junctions, i.e., alpha-caterin, beta-catenin and actin filaments, closely paralleled M-cadherin appearance and colocalized with M-cadherin in the mature glomeruli. M-cadherin, which appears as a molecular marker of glomerulus maturation, might be implicated in the formation, and be the ligand, of adherens junctions encountered in this structure.

Actins↗
PubMed1998

Endothelial cell integrin laminin receptor expression in multiple sclerosis lesions.

Laminin, a major glycoprotein component of vessel basement membranes, is recognized by beta1- and beta3-integrins expressed on endothelial cells. To determine how endothelial cell integrins might function in multiple sclerosis (MS) lesions, integrin laminin receptors and laminin were analyzed in central nervous system samples from MS patients and controls by immunohistochemistry. In active MS lesions, endothelial cell VLA-6 and beta1 subunits were decreased compared to controls whereas alpha(v) subunit and VLA-1 were increased. In chronic inactive lesions beta1, VLA-6 and alpha(v) were the same as controls but VLA-1 remained increased. Alpha3 subunit was constant in all samples. By immunoelectron microscopy VLA-1, VLA-6, beta1, and laminin were distributed throughout endothelial cells; alpha(v) was adjacent to and on luminal surfaces; alpha(v) and VLA-1 were on intercellular junctions. These results indicate distinct regulation and functions of these integrins in different lesion stages. In active lesions decreased endothelial cell beta1/VLA-6 could result in their detachment from laminin thereby facilitating leukocyte transvascular migration and blood-brain barrier breakdown. Alpha(v) and VLA-1 on intercellular junctions may participate in re-establishing vessel integrity after leukocyte migration. Luminal surface alpha(v) also likely binds intraluminal ligands and cells. In chronic inactive plaques persistently elevated endothelial cell VLA-1 correlates with long-standing endothelial cell and blood-brain barrier dysfunction.

Adolescent↗
PubMed1992

Shigella flexneri enters human colonic Caco-2 epithelial cells through the basolateral pole.

The commonly accepted view that enteroinvasive bacteria enter cells of the intestinal epithelial lining through the apical surface can be challenged in the case of shigellosis. This study is based on in vitro experiments that showed that the invasion of human colonic Caco-2 cells by Shigella flexneri occurred through the basolateral pole of these cells. In these experiments, the few bacteria that interacted with the apical surface either bound to microvilli of the cell dome without causing detectable alteration or bound at the level of intercellular junctions at which they demonstrated a limited capacity for paracellular invasion, which permitted subsequent entry through the lateral domain of the cells. Treatment of Caco-2 cell monolayers with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), which disrupts intercellular junctions, greatly enhanced the rate of cell infection. These observations suggest a physiopathological paradox that may have important consequences for the understanding of the process of colonic invasion in vivo during shigellosis.

Bacterial Adhesion↗
PubMed2005

Membranes for biohybrid liver support: the behaviour of C3A hepatoblastoma cells is dependent on the composition of acrylonitrile copolymers.

Co-polymers based on acrylonitrile, N-vinylpyrrolidone, aminoethylmethacrylate and sodium methallylsulfonate were used to prepare flat membranes by phase inversion. The surface properties of membranes were characterised by water contact angle measurements, atomic force microscopy and X-ray photoelectron spectroscopy (XPS). Membrane permeability was estimated by porosity measurements with water as test liquid. Human C3A hepatoblastoma cells were plated on these materials. Cell-material interaction was characterised by overall cell morphology, formation of focal adhesion contacts and intercellular junctions. Furthermore, cell proliferation was measured and compared with the functional activity of cells as indicated by 7-ethoxycoumarin-O-deethylation. More hydrophilic materials reduced spreading of cells, formation of focal adhesion and subsequent proliferation while homotypic cell adhesion was facilitated in correlation with stronger expressions of intercellular junctions and improved functional activity. In contrast, membranes with stronger adhesivity enhanced cell proliferation but reduced the functional activity of cells. It was concluded that the co-polymerisation of acrylonitrile with hydrophilic co-monomers, such as N-vinylpyrrolidone, could be used to tailor membrane materials for the application in biohybrid liver support systems.

Acrylonitrile↗
PubMed1995

Reappearance and long-term maintenance of connexin32 in proliferated adult rat hepatocytes: use of serum-free L-15 medium supplemented with EGF and DMSO.

Intercellular communication, especially gap junctional communication, is thought to be one of the highly differentiated functions of hepatocytes. In primary cultures of rat hepatocytes, it has been considered that the maintenance and the reinduction of differentiated functions is very difficult. In the present study, we succeeded in inducing the gap junctional protein connexin32 (Cx32) in adult rat hepatocytes cultured in serum-free L-15 medium supplemented with epidermal growth factor (EGF) and dimethylsulfoxide (DMSO). When the hepatocytes were cultured in L-15 medium supplemented with 20 mM NaHCO3 and 10 ng/ml EGF in a 5% CO2:95% air incubator, the cells proliferated. Fluorescence immunocytochemistry showed spots immunoreactive to Cx32 on the cell membranes between adjacent cells until day 3, but only a few Cx32-positive spots were found after day 4. Western and northern blot analyses also showed that the amounts of both the protein and mRNA of Cx32 in the cells decreased with time in culture. However, when the cells were treated with 2% DMSO from day 4, the immunoreactive spots reappeared on the cell membranes from day 6 and both their number and intensity gradually increased. The reappearance of Cx32 was accompanied by increases in both the protein and mRNA of Cx32. Furthermore, the expression of Cx32 was well maintained, together with extensive gap junctional intercellular communication, for more than 4 weeks. In addition, ultrastructurally, many gap junctional structures were observed between the hepatocytes, and the antibodies to Cx32 were shown to bind to those structures. This culture system may be useful for studies of the reconstruction of the gap junctional structure, the intracellular pathways of the proteins, and the regulation of synthesis and processing in differentiated hepatocytes.

Animals↗
PubMed2005

Morphological study of the interaction between M21 melanoma and lymphatic endothelium.

In order to study the interaction between melanoma and lymphatic endothelial cells (LECs) and to investigate the mechanism of lymphatic metastasis, M21 melanoma cells were seeded on the confluent LECs monolayer and the alterations of both cells were observed. The results showed that tumor cells could both adhere by pseudopodia to LECs at the site near the intercellular junction and on the apical surface. The adhesion of the melanoma cells induced the endothelial junction dissolution and endothelial retraction, which allowed the passage of the tumor cells through the opened gap and attached to the subendothelial matrix, then the tumor cells invaded and migrated under the LECs monolayer. These findings suggest that tumor cells could metastasize through the lymphatic vessel by destroying intercellular junctions or the LECs directly.

Animals↗
PubMed1972

Peroxidase arthritis. II. Lymphoid cell-endothelial interactions during a developing immunologic inflammatory response.

The interaction of lymphoid cells with vascular endothelium was studied during the development of immunologic synovitis in response to repeated intraarticular injections of a heterologous protein antigen. Lymphoid cells emigrated in venules and small veins, both by penetrating the endothelial cytoplasm and by traversing intercellular junctions. Frequent endothelial mitoses were coincident with lymphoid cell emigration. Endothelial cells in the involved vessels increased in number and bulged prominently into the vascular lumen. Endothelial nuclei contained dispersed chromatin and prominent nucleoli; the cytoplasm contained many vacuoles and abundant polyribosomes and rough-surfaced endoplasmic reticulum. Intercellular junctions were numerous and complex. These phenomena were prominent in rabbits studied after 12 to 16 daily injections; they then receded, despite continued antigenic stimulation. In animals studied after 35 or 37 daily injections, the venules appeared relatively normal, and lymphoid cell emigration was observed infrequently. Growth of new vessels was prominent at this stage. The present data do not establish whether the endothelial changes were the cause or the result of lymphoid cell emigration, although the latter seems more likely. Further studies are needed to elucidate the exact nature of these interactions.

Animals↗
PubMed2000

Dephosphorylation and intracellular redistribution of ventricular connexin43 during electrical uncoupling induced by ischemia.

Electrical uncoupling at gap junctions during acute myocardial ischemia contributes to conduction abnormalities and reentrant arrhythmias. Increased levels of intracellular Ca(2+) and H(+) and accumulation of amphipathic lipid metabolites during ischemia promote uncoupling, but other mechanisms may play a role. We tested the hypothesis that uncoupling induced by acute ischemia is associated with changes in phosphorylation of the major cardiac gap junction protein, connexin43 (Cx43). Adult rat hearts perfused on a Langendorff apparatus were subjected to ischemia or ischemia/reperfusion. Changes in coupling were monitored by measuring whole-tissue resistance. Changes in the amount and distribution of phosphorylated and nonphosphorylated isoforms of Cx43 were measured by immunoblotting and confocal immunofluorescence microscopy using isoform-specific antibodies. In control hearts, virtually all Cx43 identified immunohistochemically at apparent intercellular junctions was phosphorylated. During ischemia, however, Cx43 underwent progressive dephosphorylation with a time course similar to that of electrical uncoupling. The total amount of Cx43 did not change, but progressive reduction in total Cx43 immunofluorescent signal and concomitant accumulation of nonphosphorylated Cx43 signal occurred at sites of intercellular junctions. Functional recovery during reperfusion was associated with increased levels of phosphorylated Cx43. These observations suggest that uncoupling induced by ischemia is associated with dephosphorylation of Cx43, accumulation of nonphosphorylated Cx43 within gap junctions, and translocation of Cx43 from gap junctions into intracellular pools.

Animals↗
PubMed1989

Ultrastructure of transport pathways in stressed synovium of the knee in anaesthetized rabbits.

1. The hydraulic conductance of the synovial lining of a rabbit knee increases greatly when intra-articular pressure (IAP) is raised above approximately 9 cmH2O (yield point). To investigate the cause, synovium was fixed in situ by perfusion at controlled IAP and prepared for transmission electron microscopy. Micrographs of synovium fixed below yield pressure (atmospheric pressure and 5 cmH2O IAP, ten joints) and above it (25 cmH2O IAP, five joints) were analysed by morphometry. 2. The discontinuous cellular lining consisted of fibroblast-like cells (67%) and macrophage-like cells (33%) separated by interstitium-filled gaps. Interstitium formed 26-36% of the surface below yield pressure. Depending on sample site the surface gaps averaged 1.9 +/- 0.2 to 2.4 +/- 0.2 microns wide below yield pressure (mean +/- S.E.M. throughout). Above yield pressure the mean gap width increased by 42-64% (P less than 0.05, analysis of variance). 3. The qualitative and quantitative composition of the lining varied with distance below the surface. In a plane 5 microns deep, the intercellular distances and interstitial area fraction were almost double those at the surface. Classic periodic collagen fibrils (diameter 50 +/- 3 nm) abounded at 5 microns depth whereas the surface interstitium was richer in Ruthenium Red-staining microfibrils (diameter 9.3 +/- 0.7 nm) associated with 93 nm period fibrous long-spacing bundles. 4. Averaging over all the tissue between the surface and the 5 microns deep plane, the mean interstitial volume fraction was 0.61 +/- 0.05 at 5 cmH2O and 0.67 +/- 0.02 at 25 cmH2O (n.s.). 5. Capillary fenestrae (8.5 +/- 1.1 per fenestrated profile) and intercellular junctions were unaltered at high IAP. The tortuosity of the capillary-to-joint cavity path was 1.50 +/- 0.01 below yield pressure and 1.86 +/- 0.24 at 25 cmH2O (n.s.). 6. Intra-articular tracers (ferrocyanide, ferritin and glycogen) permeated synovial interstitium without evidence of preferential pathways. Ferrocyanide delineated the capillary intercellular junction as a permeable channel. Ferritin and glycogen were phagocytosed by the macrophages. 7. In suprapatellar areolar synovium, the most extensive and most altered tissue, the ratio of interstitial area to path length increased maximally 4.1 times between 5 and 25 cmH2O IAP. This represents a substantial contribution to the physiologically estimated rise in interstitial conductance (14 x) but does not wholly explain it.

Animals↗
PubMed1981

[Human aorta: endothelium and atheroma (author's transl)].

An electron microscopic study of aortic endothelium obtained from necropsy and biopsy material shows pathological changes corresponding the severity of the atheromatous state, but unrelated to age. All stage I aortas show the same type of endothelial changes. So do stage II aortas. The pathological structural changes in the endothelial cells corresponding to aortas of stage I, II-III involve the microfilaments, vesicles, intercellular junctions and basement membrane. The microfilaments are more numerous and better defined in atheromatous aortas. Also rare bundles of microfilaments with electron-dense centers are seen. The intra-cytoplasmic vesicles increase presently deeper invaginations (pseudo-channels) in the stages II and III aortas. In these stages the intercellular junctions are open involving all or part of the junctions. All three described ultra-structural changes increase the permeability of the endothelium to lipids and plasma glycoproteins. The thickening of the sub-endothelial basement membrane résults from the increase of type IV collagen synthesized by the endothelial cells. Lysis of endothelial cells and platelet agregation are related to the stage of atheromatosis. The number of Weibel Palade bodies increase in stade II and III aortas. These organelles play a role in blood coagulation and accelerate atheromatosis. In conclusion, the aortic endothelium constitutes an active barrier. The pathological atheromatosis process involves the endothelium. The endothelial cells play a normal role in the passage of molecules from blood plasma into the aortic wall. That explains intimal formation and intimal fibrosis. The endothelium also participates in the initial pathogenic mechanism of atheroma formation (fatty dot and streak, gray gelatinous elevation and mural thrombus).

Aging↗
PubMed2002

Twenty percent alcohol toxicity on rabbit corneal epithelial cells: electron microscopic study.

PURPOSE: To evaluate 20% ethanol toxicity on the rabbit corneal epithelium, ethanol-treated rabbit corneas were examined with electron microscopy. METHODS: Rabbit corneas (24 eyes) were treated with 20% ethanol for 30 seconds, 1 minute, and 2 minutes by using LASEK (laser-assisted subepithelial keratectomy) instruments and then washed with sterile water. Zero time, 1, 3, 5 days after ethanol treatment, corneas were excised and examined with scanning and transmission electron microscopy (SEM and TEM). RESULTS: Widespread partial or total damage of microvilli, focal breaks of intercellular junction, and cellular edema was observed. The damage was more severe in corneas with longer ethanol treatment. In corneas with ethanol treatment more than 1 minute, slough of superficial corneal epithelium occurred and progressed with time. Two-minute ethanol treatment resulted in complete destruction of microvilli and significant separation of intercellular junction. These pathologic changes persisted 5 days after ethanol treatment. CONCLUSIONS: From these results, increasing exposure time to ethanol more than 1 minute results in significant damage to superficial corneal epithelium and prolongs its normal recovery time.

Animals↗
PubMed2005

[Gap junction-mediated intercellular communication in astrocytes and neuroprotection].

Neuroglial interaction represents a concept that is now more and more integrated in the attempts to understand who does what and how in neuronal processing and survival, in normal as well as in pathological situations. The purpose of the review is to provide an overlook about the role of glial cells, mainly astrocytes, in neuroprotection. Since a typical feature of glia is to be connected by gap junctions that allow them to be organized as a communicating network(s), we will focus this review on what is known about the contribution of astrocyte gap junctions (AGJ) in neuronal survival. As neuroglial interaction and AGJ are both affected during neurodegenerative diseases, we will also consider the above mentioned glial properties in a pathological context with a special interest in Alzheimer's disease.

Alzheimer Disease↗
PubMed1999

[Effect of ATP on malignant phenotype of a human gastric cancer cell line].

OBJECTIVE: To study the effect of ATP on proliferation and differentiation of a human gastric cancer cell line. METHODS: M17, a subclone of human gastric cancer cell line MGC-803, was treated in vitro with ATP(0.23 mg/ml). After 48 hr, the following parameters were examined. (1) Proliferation of cells by daily cell counting. (2) Microvilli of the cells were observed by scanning EM. (3) Gap junction intercellular communication was examined by mechanical scraping and Lucifer dye transfer. (4) Microfilament of the cytoskeleton was studied with fluorescin-labeled phalloidin. (5) Vinculin adhesion plague was stained immunocytochemically with monoclonal antibodies. RESULTS: ATP significantly inhibited the in vitro growth of M17 cells. The ATP-treated M17 cells showed disappearance of microvilli on the cell surface, increased gap junction intercellular communication, improved organization of microfilament bundles and reappearance of vinculin adhesion plagues. CONCLUSION: ATP not only inhibits proliferation but also induces differentiation of a human gastric cancer cell line with reversion from malignant toward normal phenotype. The parameters examined could serve as useful biomarkers of human gastric cancer.

Actin Cytoskeleton↗
PubMed2002

Actin cable dynamics and Rho/Rock orchestrate a polarized cytoskeletal architecture in the early steps of assembling a stratified epithelium.

To enable stratification and barrier function, the epidermis must permit self-renewal while maintaining adhesive connections. By generating K14-GFP-actin mice to monitor actin dynamics in cultured primary keratinocytes, we uncovered a role for the actin cytoskeleton in establishing cellular organization. During epidermal sheet formation, a polarized network of nascent intercellular junctions and radial actin cables assemble in the apical plane of the monolayer. These actin fibers anchor to a central actin-myosin network, creating a tension-based plane of cytoskeleton across the apical surface of the sheet. Movement of the sheet surface relative to its base expands the zone of intercellular overlap, catalyzing new sites for nascent intercellular junctions. This polarized cytoskeleton is dependent upon alpha-catenin, Rho, and Rock, and its regulation may be important for wound healing and/or stratification, where coordinated tissue movements are involved.

Actin Cytoskeleton↗