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PubMed1975

Junctional complexes of the tubular cells in the human kidney as revealed with freeze-fracture.

Intercellular junctions between human kidney tubular cells were studied by the freeze-fracture technique. The number of strands of the zonulae occludentes increased gradually from the proximal segment to the collecting tubule. Only one strand was visible in the proximal segment (in contrast to 2-4 strands of the neighbouring Bowman's capsule). In the thin segment 2-4 strands were revealed. In the distal segment 1-5 strands were present in the pars recta, 4-6 in the pars convoluta. The most extensive and complex zonulae occludentes were found in the collecting tubule. Gap junctions were seen only between proximal tubular cells. The extent of the zonulae occludentes along the tubules in human kidneys is very similar to that observed in the kidney tubules of other mammals. The findings accord well with electrophysiological measurements and with the results of tracer studies on experimental animals.

Adult↗
PubMed1998

Regulation of the movement of solutes across tight junctions.

The intercellular tight junction is the rate-limiting barrier in the paracellular pathway for permeation by ions and larger solutes. A variety of widely used electrical and flux approaches are used in the analyses of solute permeation through this pathway; however, each has limitations in practice. It is now clear that solute permeation across tight junctions is dynamically regulated by intracellular events with a common effector mechanism apparently tied to the cytoskeleton. These pathways, which regulate tight junction solute permeability, are targets that produce epithelial barrier dysfunction in a variety of disease states. However, regulation of solute permeation across the junctional barrier may also represent a potential means to improve bioavailability of orally administered bioactive solutes.

Animals↗
PubMed1992

Endothelial cells: adhesion and tight junctions.

This article reviews recent discoveries concerning the identity of endothelial cell adhesion molecules and their participation in intercellular junction formation. Observations relating to the formation of high-resistance tight junctions between brain endothelial cells are emphasized.

Animals↗
PubMed1992

Hormonal regulation of intercellular communication: parathyroid hormone increases connexin 43 gene expression and gap-junctional communication in osteoblastic cells.

The presence of gap junctions between osteoblastic cells has been previously reported. For this study we used the rat osteosarcoma cell line UMR 106, which expresses the osteoblastic phenotype, as a model to characterize further the nature, physiology, and regulation of gap junctions. Northern blot analysis identified a 3.0-kilobase RNA species corresponding to the gap junction protein connexin 43. The presence of two other connexin RNA species (26 and 32) could not be detected by this method in these cells. The identified connexin RNA was amplified by reverse transcription coupled to polymerase chain reaction; the sequence of the amplified product appears identical to the sequence of a cloned rat heart connexin 43 gene. After treatment with PTH, forskolin, and 8-Br-cAMP (a cAMP analog), the levels of connexin 43 RNA in UMR 106 cells increased. Further evidence for the role of PTH and cAMP in the physiology of gap junctions in these cells was obtained with Lucifer yellow dye transfer experiments. Gap-junctional intercellular communication increased in response to PTH and forskolin (an inducer of adenylate cyclase activity). Expression of connexin 43 RNA increased severalfold in response to PTH in a concentration- and time-dependent fashion. Connexin 43 RNA and its PTH-mediated stimulation were also observed in several other osteoblastic cell lines. The roles of PTH and forskolin in regulating the physiological state of gap junctions were confirmed in primary cultures of rat calvaria osteoblasts.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Reorganization of cytoskeletal and junctional proteins during cochlear hair cell degeneration.

Experiments were carried out to elucidate changes in cytoskeletal elements and intercellular junctions in the organ of Corti, when hair cells degenerate and phalangeal scars form. Hair cell damage was induced by exposing guinea pigs to high intensity noise. The spatial and temporal changes in the organization of microfilaments, intermediate filaments, and tight junction-specific proteins were investigated using scanning and transmission electron microscopy and histochemistry. The results show that microfilaments, cytokeratins, adherens junctions, and tight junctions rearrange their distribution in damaged areas. From the temporal sequence of these changes it appears that phalangeal scars develop simultaneous with hair cell degeneration, and that the integrity of the luminal membranes in the organ of Corti is not interrupted. Each scar is formed by two supporting cells which expand and invade the sub-apical region of the dying hair cell. This region becomes cytokeratin-positive. The two supporting cells meet at the mid-line of the scar, where a new junctional complex is formed. The junctional complex consists of tight junction and adherens-type junction, but desmosomes are absent.

Actins↗
PubMed1974

Development of junctions during differentiation of lens fibers.

Throughout the differentiation of eye lens epithelium into fibers, an extensive system of intercellular junctions develops. The junctional assembly is initially characterized by the accumulation of 9.0-nm intramembranous particles, forming linear rows in the matching plasma membranes of adjoining fibers. At the final stage of the fiber differentiation, the junctional particles are assembled in geometrically packed arrays. The formation of linear rows and bidimensional lattices of intramembranous particles probably favors reciprocal recognition of cell surfaces and specific cell-to-cell interlocking. Moreover, the existence of a rather rigid lipid core of the plasma membrane of eye lens fiber may promote the clustered distribution of intramembranous particles and facilitate the junctional assembly.

Animals↗
PubMed1991

Penetration of lanthanum through the main pancreatic duct epithelium in cats following exposure to infected human bile.

The main pancreatic duct epithelium acts as a barrier to the diffusion of molecules from the duct lumen into pancreatic acinar and interstitial tissue. We studied sequential ultrastructural characteristics of the loss of epithelial barrier function in the cat using lanthanum, an electron-opaque tracer, following perfusion of the duct from the tail to the duodenum with infected human bile. Tight junctions between duct epithelial cells were found to become permeable to the tracer as early as after 15 min of exposure. Later, there was progressive disintegration of intercellular junctions and epithelial loss. Lanthanum penetrated the duct epithelium exclusively on an intercellular path. Loss of barrier function of the pancreatic duct epithelium was consistently associated with subsequent development of acute interstitial edematous pancreatitis. There was no association between the degree of duct epithelial damage and the severity of acute pancreatitis. Both bile and a suspension of bacteria alone were not harmful to the pancreas. Sequential perfusion produced acute pancreatitis only when at first bile and then the bacterial suspension was perfused. A reversed succession of perfusates produced no morphologic alterations. We conclude: (1) Increased tight junction permeability is an early lesion in acute bile-induced pancreatitis: (2) loss of duct epithelial barrier function is important for the initiation but not for the severity of the inflammation; and (3) bile renders duct epithelial intercellular junctions vulnerable to Escherichia coli bacteria.

Acute Disease↗
PubMed1975

Complex tight junctions of epithelial and of endothelial cells in early foetal brain.

?The morphology of epithelial and of endothelial intercellular junctions in human foetal (9-15 weeks gestation) and sheep foetal (50, 60 and 125 days gestation, term 147 days) brain has been studied using the freeze-fracture technique and thin section transmission electronmicroscopy. Freeze-fracture replicas of the choroid plexus of both early human and sheep foetuses showed that the choroidal ependymal cells are linked at the ventricular surface by tight junctions. Freeze-fracture replicas of foetal cortical endothelial cell junctions showed that they are still more complex than those of choroidal epithelial cells, in all specimens so far examined. In some 60 day sheep foetuses the dye Alcian blue, which binds to plasma albumin and which iselectrondense when treated with osmium tetroxide, was injected intravenously a few minutes prior to fixation. The dye penetrated from blood into brain extracellular space and c.s.f. but apparently not by an intercellular route. The dye was found in a tubular system (endoplasmic reticulum) in both choroidal epithelial and cortical endothelial cells. The possibility that protein penetrates into the foetal brain and c.s.f. by a transcellular route is discussed. The possible significance of these findings in relation to previous ideas and studies of the development of blood-brain barrier mechanisms is also considered.

Animals↗
PubMed1982

Domain turnover of junctional membrane areas in the epidermis.

To investigate the turnover of complete junctional membrane areas ("domain turnover"), psoriatic epidermis, keratoacanthoma, and squamous cell carcinoma were studied with an electron microscope and compared with the normal epidermis. Three types of domain turnover of junctions were observed. First, the uptake of intact intercellular junctions, which occurred as complete or incomplete annular junctions in the cytoplasm. Mainly gap junctions were involved. Second, the formation of autojunctions bridging an infolding at the surface of a cell, which is then incorporated and occurs partly with an attached saccule in the cytoplasm. This type was confined to desmosomes. Finally, the loss of intercellular desmosomes into the intercellular space was observed. Proliferating epidermis was associated with an increased domain turnover of gap junctional membrane areas. Domain turnover of desmosomes prevailed in tumors.

Carcinoma, Squamous Cell↗
PubMed1988

Development, organization, and function of tight junctional complexes in the tracheal epithelium of infant ferrets.

The surface epithelium of newborn ferret airways matures rapidly in the first month of life. Prominent developmental features include a transition from predominantly non-ciliated to ciliated cells, quantitative and qualitative changes in secretion of macromolecules, and a transition from secretory to absorptive patterns of ion transport. Freeze-fracture replicas of ferret tracheal epithelium from 0 to 28 days of age exhibited progressive developmental patterns in tight junctional structure from beaded, unclosed patterns in newborns to more closed patterns at 28 days. Strand number increased while the depth of tight junctional structures and the proportion of strands exhibiting discontinuity decreased postnatally. Total transepithelial conductance, paracellular conductance, and cell size decreased over the first month. Our data suggest that changes in physiological parameters that reflect epithelial tight junction permeability can be attributed, at least in part, to maturation of this intercellular junction during the postnatal period.

Animals↗
PubMed1979

Gap junctions between microvilli of an oocyte and follicle cells in the teleost (Plecoglossus altivelis).

In the teleost, Plecoglossus altivelis, intercellular junctions between microvilli of an oocyte and follicle cells were studied by electron microscopy. Microvilli, which were radiated from an oocyte and arrived at the surface of follicle cells, established contact with follicle cells. These contact areas appeared to be a seven-layered membrane with an overall thickness of about 18 microns by standard fixation. In freeze-fracture replicas, many small aggregates of intramembraneous particles were revealed on the cleavage faces of cytoplasmic membranes of follicle cells. These morphological evidences suggest that in the teleost gap junctions exist between the oocyte and follicle cells, especially on the surface of follicle cells.

Animals↗
PubMed1995

Regulated assembly of tight junctions by protein kinase C.

We have previously shown that protein phosphorylation plays an important role in the sorting and assembly of tight junctions. We have now examined in detail the role of protein kinases in intercellular junction biogenesis by using a combination of highly specific and broad-spectrum inhibitors that act by independent mechanisms. Our data indicate that protein kinase C (PKC) is required for the proper assembly of tight junctions. Low concentrations of the specific inhibitor of PKC, calphostin C, markedly inhibited development of transepithelial electrical resistance, a functional measure of tight-junction biogenesis. The effect of PKC inhibitors on the development of tight junctions, as measured by resistance, was paralleled by a delay in the sorting of the tight-junction protein, zona occludens 1 (ZO-1), to the tight junction. The assembly of desmosomes and the adherens junction were not detectably affected, as determined by immunocytochemical analysis. In addition, ZO-1 was phosphorylated subsequent to the initiation of cell-cell contact, and treatment with calphostin C prevented approximately 85% of the phosphorylation increase. Furthermore, in vitro measurements indicate that ZO-1 may be a direct target of PKC. Moreover, membrane-associated PKC activity more than doubled during junction assembly, and immunocytochemical analysis revealed a pool of PKC zeta that appeared to colocalize with ZO-1 at the tight junction. A preformed complex containing ZO-1, ZO-2, p130, as well as 330- and 65-kDa phosphoproteins was detected by coimmunoprecipitation in both the presence and absence of cell-cell contact. Identity of the 330- and 65-kDa phosphoproteins remains to be determined, but the 65-kDa protein may be occludin. The mass of this complex and the incorporation of ZO-1 into the Triton X-100-insoluble cytoskeleton were not PKC dependent.

Animals↗
PubMed1986

Junctional complexes of the in vitro developed inner ear. A freeze fracture study.

The freeze fracture technique was used to study intercellular junctions of inner ear anlages developed in vitro. The 16th gestational day inner ear from the CBA/CBA mouse was cultured for 5 days whereafter the specimens were analyzed. Inner ears developed in vivo were used as controls. A considerable variation in the maturation of the tight junctional complexes occurred in both the vestibular and cochlear parts of the labyrinth. The sequential maturation of tight junctions and gap junctions showed the same structural features in the in vivo and the in vitro developed inner ears, although it seemed that the in vivo developed inner ears showed a slightly more overall mature morphology of tight junctions.

Animals↗
PubMed1991

Junctional systems in the pineal gland of the Wistar rat (Ratus ratus). A freeze-fracture and thin section study.

Intercellular junctions between neighbouring pinealocytes, glial cells, glial cells and pinealocytes as well as between nerve endings and parenchymal cells of the pineal gland of Wistar rats were investigated on freeze-fracture replicas and thin sections by transmission electron microscopy. Gap junctions, tight junctions and the annular gap junctions have been revealed. In addition, chemical synapses between nerve endings and pinealocytes have been observed.

Animals↗
PubMed2000

Signal transduction pathways in enhanced microvascular permeability.

We have been investigating the molecular mechanisms underlying pathophysiological regulation of microvascular permeability on isolated venules and cultured venular endothelial monolayers. Physiological approaches have been employed in combination with molecular analyses to probe the signal transduction pathways leading to enhanced microvascullar permeability. A newly developed technique of protein transfection into cells and intact microvessels enables the correlation of fullctional reactions and signaling events at the molecular level in a direct and specific fashion. The results indicate that inflammatory mediators increase microvascular permeability via intracellular signaling pathways involving the activation of phospholipase C, cytosolic calcium, protein kinase C, nitric oxide synthase, guanylate cyclase, and protein kinase G. In response to the signaling stimulation, complex biochemical and conformational reactions occur at the endothelial structural proteins. Specifically, myosin light-chain activation-mediated myosin light-chain phosphorylation can result in cell contraction. VE-cadherin and beta-catenin phosphorylation may induce dissociation of the junctional proteins and their connection to the cytoskeleton, leading to a loose or opened intercellular junction. Focal adhesion phosphorylation and redistribution further provide an anchorage support for the conformational changes in the cells and at the cell junction. The three processes may act in concert to facilitate the flux of fluid and macromolecules across the microvascular endothelium.

Animals↗
PubMed1984

A quantitative study of intramembrane changes during cell junctional breakdown in the dystrophic rat retinal pigment epithelium.

Previous electron microscope freeze-fracture and tracer studies have revealed that intercellular junctions in the retinal pigment epithelium (RPE) of Royal College of Surgeons (RCS) rats with inherited retinal dystrophy [5] break down between three and six postnatal weeks [6, 7]. In this study quantitative computer techniques were used to analyze the freeze-fracture changes in the dystrophic RPE. The following parameters were measured: length of tight junctional strands/micron2; number of tight junctional strand anastomoses/micron2; number of gap junctional aggregates/micron2; area of gap junctional aggregates/micron2; and density of background intramembrane particles/micron2. At three postnatal weeks, the dystrophic junctional complex membrane is similar to normal, but at 10 weeks and later there are dramatic decreases in tight junctional strand length/micron2 and number of anastomoses/micron2, as well as in the number/micron2 and area of gap junctions/micron2, while the density of background particles/micron2 is dramatically increased. Correlational analysis revealed that changes in gap and tight junctions were significantly related to each other and to the increase in background particle density. The diameter of background particles within the normal and post-breakdown dystrophic junctions was measured in order to see whether the dispersal of gap and tight junctional particles (8-10 nm) into the surrounding membrane contributes to the increased particle density. These measures showed that background particles in all size ranges were more numerous in the dystrophic RPE, but that the largest increase was in the smallest diameter particles (6-7 nm). Thus, while gap and tight junctional sized particles contribute to the increase, particles from other sources may also be involved. Particle density of apical and basal membranes in the normal and in the 10 week and older dystrophic RPE was analyzed to study the effects of tight junctional breakdown on the distribution of intramembrane particles. These measures showed that particle density was greater basally than apically in the normal RPE and that particle density in both membranes decreased slightly in the dystrophic RPE, but that their ratio remained unchanged. It has been shown previously that even a single intact tight junctional strand is sufficient to maintain differences in particle density between apical and basal surfaces [14, 15] and in the majority of abnormal dystrophic junctional complexes at least one tight junctional strand remains intact.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1977

Ultrastructure of a cardiac rhabdomyoma.

Electron microscopic study of a cardiac rhabdomyoma removed at open heart operation revealed large rounded or polygonal cells that contained large amounts of monoparticulate glycogen. Myofibrils in these cells were few and located either subjacent to the plasma membranes or radiating from central areas. Leptofibrils and masses of anomalous Z band material were abundant. Shallow tubular sarcolemmal invaginations and elements of free and junctional sarcoplasmic reticulum were associated with the myofibrils. Desmosomes and nexuses were evident in intercellular junctions, which were extensive and randomly distributed throughout the cell surfaces. It is concluded that cardiac rhabdomyomas probably are hamartomas.

Cell Membrane↗
PubMed1993

Intercellular communication in colonies of Syrian hamster embryo cells and the susceptibility for morphological transformation.

The levels of gap junctional intercellular communication (GJIC) were studied in normal, morphologically altered and morphologically transformed colonies formed in the Syrian hamster embryo (SHE) cell transformation assay. The colonies were selected from non-exposed dishes or dishes exposed to 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.16 microM), di(2-ethylhexyl)phthalate (DEHP, 77 microM), Na-orthovanadate (vanadate, 3.4 microM) or dieldrin (25 microM) for 7 days during colony formation. TPA, DEHP and vanadate induced increased frequencies of morphological transformation of colonies. At the same time, TPA and DEHP decreased GJIC in the colonies by approximately 30% under the conditions used. All categories of colonies were equally affected. Vanadate did not change the level of GJIC in any of the categories of colonies compared to unexposed control. Dieldrin strongly suppressed GJIC in all colonies without increasing the frequency of transformation. The compounds affected GJIC after short-term exposures (4 and 24 h) to cell monolayers rather similarly to that found after long-term exposure to the colonies. Transformation assays with coexposure of dieldrin together with the transforming agents vanadate, DEHP or benzo[a]pyrene did not increase transformation frequencies compared to the transforming agents alone. The GJIC level in all coexposure groups was similar to that of dieldrin alone. Furthermore, regardless of whether dieldrin was present or not, removal of vanadate 24 h before fixation of the colonies caused a slight decrease in the transformation frequency. The results suggest that: (i) morphologically transformed colonies have the same ability of intercellular communication as normal colonies; (ii) decreased GJIC is probably not either sufficient or necessary to induce transformation of SHE cell colonies; (iii) a decreased level of GJIC does not necessarily increase the susceptibility of SHE cells for transformation; and (iv) inhibition of GJIC may not have an impact on the maintenance of the transformed phenotype of SHE cell colonies.

Animals↗