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PubMed1988

The modulation of cell adhesion molecule expression and intercellular junction formation in the developing avian inner ear.

The cells that constitute the membranous labyrinth in the vertebrate inner ear are all derived from a single embryonic source, namely, the otocyst. The mature inner ear epithelia contain different regions with highly differentiated cells, displaying a highly specialized cytoarchitecture. The present study was designed to determine the presence of adherens-type intercellular junctions in this tissue and study the expression of cell adhesion molecules (CAMs) associated with these junctions, namely, A-CAM and L-CAM, in the developing avian inner ear epithelia. The results presented here show that throughout the early otocyst, A-CAM is coexpressed with L-CAM. The formation of asymmetries between sensory and nonsensory areas in the epithelium is accompanied by the modulation of CAMs expression and the assembly of intercellular junctional complexes. A-CAM and L-CAM display reciprocal expression patterns, the former being expressed mostly in the mosaic sensory epithelium, while L-CAM becomes conspicuous in the nonsensory areas but its expression in the sensory region is markedly reduced. Adherens-type junctions and numerous desmosomes are found in the junctional complexes of early otocyst cells. The former persist to maturity of the various inner ear epithelia, whereas desmosomes disappear from junctional complexes of hair cells but remain in the intercellular junctional complexes of all other cell types in the membranous labyrinth. Thus, adherens type intercellular junctions comprise the only defined cytoskeleton-bound junction in mature hair cells. A-CAM-positive cells are also found in the region of the acoustic ganglion in early developmental stages but not in the mature neural elements.

Actins↗
PubMed2005

Intercellular junctions in Ewing sarcoma/primitive neuroectodermal tumor: additional evidence of epithelial differentiation.

Ewing sarcoma/primitive neuroectodermal tumor (ES/PNET) has recently been shown to frequently express cytokeratins, suggesting partial epithelial differentiation. Older ultrastructural studies have documented primitive cell-cell junctions in ES/PNET, reportedly resembling poorly formed desmosomes. Recently, paraffin-reactive antibodies have become available to proteins found in a variety of intercellular junctions indicative of epithelial differentiation, including tight junctions, desmosomes and adherens junctions. We examined intercellular junction protein expression in a large number of genetically confirmed ES/PNET. Formalin-fixed, paraffin-embedded sections from 23 primary and seven recurrent or metastatic cases of genetically confirmed ES/PNET were immunostained for claudin-1 and occludin (tight junction structural proteins), zonula occludens-1 (ZO-1, tight junction linker protein), desmoglein 1/2 (desmosomal adherens protein), desmoplakin (desmosomal structural protein) and E-cadherin (epithelial adherens junction protein), using steam heat-induced epitope retrieval and the Dako Envision system. Cases with >5% positive cells were scored as 'positive'. Normal colonic epithelium and skin served as external positive controls. Claudin-1 was expressed by 19 of 30 specimens (63%), ZO-1 was expressed by 15 of 29 specimens (51%), and occludin was expressed by three of 28 specimens (11%). In 28 specimens all three tight junction markers were evaluable. In all, 15 samples (54%) expressed only one tight junction marker, and 10 samples (36%) expressed two tight junction markers. No case expressed all three tight junction markers. Desmoglein was expressed in one of 30 (3%) samples. Desmoplakin was expressed in two of 28 (7%) samples. E-cadherin was negative in all cases. Our data suggest that many of the previously described cell-cell junctions in ES/PNET are poorly formed tight junctions, given the high frequency of claudin-1 and ZO-1 expression. This may underestimate the true frequency of tight junction protein expression in ES/PNET, as there are at least 20 different claudins and other ZO proteins. These tight junctions are almost certainly abnormal, given the absence of occludin expression in most cases. Desmosomal and adherens junction protein expression was rare to absent. Our findings provide additional evidence that ES/PNET frequently show partial epithelial differentiation.

Bone Neoplasms↗
PubMed1997

Stimulation of cell proliferation and inhibition of gap junctional intercellular communication by linoleic acid.

The effect of linoleic acid (LA) on gap-junction permeability, connexin 43 mRNA level, protein level, and phosphorylation, and the numbers of gap-junctional membrane plaques were studied in the rat liver epithelial cell line WB-F344 to determine whether changes in these parameters correlated with the enhanced cell growth and the inhibition of gap-junction function. When cultured in a medium with low serum (1%), these cells exhibited a slower growth rate than in the high serum medium (7%). Addition of linoleic acid (0.01-3 mg/ml) to the low serum medium increased the growth rate and inhibited gap junctional intercellular communication (GJIC) in a dose-dependent manner. In a comparison of short-term and long-term treatments with LA, GJIC in short-term treated (1 h) WB cells was inhibited at 3 mg/ml LA but readily recovered by washing and removing LA from cells, whereas GJIC in long-term treated (6 days) WB cells did not recover by washing and removing LA from WB cells. Western blot analysis of connexin 43 showed that a short-term incubation with linoleic acid increased the relative amount of unphosphorylated connexin 43 protein, but a long-term incubation with linoleic acid decreased the amount of unphosphorylated connexin 43 protein and increased the relative amount of hyperphosphorylated connexin 43 protein. Connexin 43 and p53 mRNA levels decreased in a time- and dose-dependent manner in linoleic acid-treated cells. These results suggest that growth stimulation and gap junctional intercellular communication inhibition of rat liver epithelial cells by linoleic acid may be mediated in part through modulation of p53 expression and function.

Animals↗
PubMed1993

Structural changes in intercellular junctions during keratinization of the stratum medium of the equine hoof wall.

Cells of the intertubular horn of the stratum medium of the equine hoof wall are joined by three types of junctions. Desmosomes and gap junctions were present in all strata. Septate-like junctions and an intercellular line were seen in the distal stratum spinosum subsequent to extrusion of the contents of membrane-coating granules. At a later stage of keratinization, non-membrane-bound acid phosphatase reaction product appeared to leak into the intercellular space except into areas occupied by septate-like junctions and the intercellular line. It is proposed that the formation of septate-like junctions and the intercellular line prior to leakage of acid phosphatase into the intercellular space created stable areas of intercellular adhesion between fully keratinized cells.

Acid Phosphatase↗
PubMedDate not supplied

Effects of neuroinflammation on glia-glia gap junctional intercellular communication: a perspective.

Gap junctions serve as intercellular conduits that allow for the direct transfer of small molecular weight molecules (up to 1 kDa) including ions involved in cellular excitability, metabolic precursors, and second messengers. The observation of extensive intercellular coupling and large numbers of gap junctions in the central nervous system (CNS) suggests a syncytium-like organization of glial compartments. Inflammation is a hallmark of various CNS diseases such as bacterial and viral infections, multiple sclerosis, Alzheimer's disease, and cerebral ischemia. A general consequence of brain inflammation is reactive gliosis typified by astrocyte hypertrophy and proliferation of astrocytes and microglia. Changes in gap junction intercellular communication as reflected by alterations in dye coupling and connexin expression have been associated with numerous CNS inflammatory diseases, which may have dramatic implications on the survival of neuronal and glial populations in the context of neuroinflammation. A review of the effects of inflammatory products on glia-glia gap junctional communication and glial glutamate release is presented. In addition, the hypothesis of a "syncytial switch" based upon differential regulation of gap junction expression in astrocytes and microglia during normal CNS homeostasis and neuroinflammation is proposed.

Animals↗
PubMed2003

The role of stem cells and gap junctional intercellular communication in carcinogenesis.

Understanding the process of carcinogenesis will involve both the accumulation of many scientific facts derived from molecular, biochemical, cellular, physiological, whole animal experiments and epidemiological studies, as well as from conceptual understanding as to how to order and integrate those facts. From decades of cancer research, a number of the "hallmarks of cancer" have been identified, as well as their attendant concepts, including oncogenes, tumor suppressor genes, cell cycle biochemistry, hypotheses of metastasis, angiogenesis, etc. While all these "hallmarks" are well known, two important concepts, with their associated scientific observations, have been generally ignored by many in the cancer research field. The objective of the short review is to highlight the concept of the role of human adult pluri-potent stem cells as "target cells" for the carcinogenic process and the concept of the role of gap junctional intercellular communication in the multi-stage, multi-mechanism process of carcinogenesis. With these two concepts, an attempt has been made to integrate the other well-known concepts, such as the multi-stage, multimechanisn or the "initiation/promotion/progression" hypothesis; the stem cell theory of carcinogenesis; the oncogene/tumor suppression theory and the mutation/epigenetic theories of carcinogenesis. This new "integrative" theory tries to explain the well-known "hallmarks" of cancers, including the observation that cancer cells lack either heterologous or homologous gap junctional intercellular communication whereas normal human adult stem cells do not have expressed or functional gap junctional intercellular communication. On the other hand, their normal differentiated, non-stem cell derivatives do express connexins and express gap junctional intercellular communication during their differentiation. Examination of the roles of chemical tumor promoters, oncogenes, connexin knock-out mice and roles of genetically-engineered tumor and normal cells with connexin and anti-sense connexin genes, respectively, seems to provide evidence which is consistent with the roles of both stem cells and gap junctional communication playing a major role in carcinogenesis. The integrative hypothesis provides new strategies for chemoprevention and chemotherapy which focuses on modulating connexin gene expression or gap junctional intercellular communication in the premalignant and malignant cells, respectively.

Cell Communication↗
PubMed1986

Reversible inhibition of intercellular junctional communication by glycyrrhetinic acid.

Intercellular gap-junctional communication was measured using metabolic co-operation in co-cultures of argininosuccinate synthetase-deficient and argininosuccinate lyase-deficient human fibroblasts. 18-alpha-glycyrrhetinic acid (AGA) was found to inhibit communication by more than 95% at concentrations as low as 2 microM. Concentrations up to 100 microM were not cytotoxic over a period of 2 hours. Communication inhibition was of rapid onset and was readily reversible. Communication remained continuously yet reversibly blocked in cells cultured in the presence of AGA for 20 days. The related compounds 18-beta-glycyrrhetinic acid and carbenoxolone also caused communication inhibition. The effect is probably not mediated via mineralocorticoid or glucocorticoid receptors since aldosterone and glucocorticoids had no effect on communication. AGA thus has properties of a useful inhibitor in the study of intercellular junctional communication.

Carbenoxolone↗
PubMed2003

Establishment of cadherin-based intercellular junctions in the dermal papilla of the developing hair follicle.

During hair follicle development, mesenchymal cells aggregate to form the dermal papilla with hair-inducing activity. However, the cellular mechanisms underlying the aggregative behavior of dermal papilla cells are less known. The present study demonstrates that cadherin-based intercellular junctions interconnect dermal papilla cells in developing hair follicles of mice. It is shown that as mesenchymal cells aggregate to be surrounded by epithelium in developing hair follicles, cadherin-11 comes to exhibit the dotted patterns of distribution. The appearance of the dot-like distribution of the molecule is concomitant with the formation of intercellular junctions in the mesenchymal aggregate, which make a tightly packed population of cells with little extracellular space. At later stages of the development, although extracellular space reappears in the dermal papilla, the cells remain interconnected by well-developed intercellular junctions, where cadherin-11 as well as beta-catenin is localized. Taking into consideration the normal hair development in cadherin-11 mutant mice, it might be that multiple cadherins are responsible for the establishment of intercellular junctions in the dermal papilla and serve to maintain the aggregative behavior of the cells.

Animals↗
PubMed1985

Inhibition of intercellular junctional communication in human fibroblasts by triphenylmethane, triphenylmethylchloride, tetraphenylboron and related compounds.

Intercellular junctional communication was measured using [14C]citrulline incorporation in co-cultures of argininosuccinate synthetase-deficient and argininosuccinate lyase-deficient human fibroblasts. Triphenylmethane, triphenylmethylchloride and tetraphenylboron inhibited communication at concentrations at least 12-fold lower than cytotoxic concentrations. This inhibition was of rapid onset and was rapidly reversible by washing the co-cultures. Refractoriness to inhibition did not develop after prolonged exposure. Several other compounds also induced communication inhibition, but only at concentrations slightly below cytotoxic concentrations. Treatment of co-cultures with calcium ionophore A23187 or cycloheximide did not cause communication inhibition. It is suggested that triphenylmethane, triphenylchloride and tetraphenylboron may be useful inhibitors for studying the roles of intercellular junctional communication in some biological systems.

Argininosuccinate Lyase↗
PubMed1979

Ultrastructure of intercellular junctions in the rat exocrine pancreas stimulated by pancreozymin.

Intercellular junctions in the exocrine pancreas, through which pancreatic enzymes may leak out from the lumen into the intercellular spaces, were studied in the rat by means of electron microscopy using tannic acid as a tracer and freeze-fracture methods as well as conventional thin sections. In thin sections and freeze-fracture replicas from the pancreas stimulated or not stimulated by exogenous pancreozymin, tight junctions were located between adjacent cells of the acinus or duct at the level just below the lumen. Observation of freeze-fracture replicas revealed that the number of strands or furrows in the tight junction did not differ significantly between the two groups but the width of the tight junction area was narrower and the distance between neighboring strands or furrows in the junction was smaller in the stimulated pancreas than in the control pancreas. Tannic acid, the molecular weight of which is smaller than that of pancreatic enzymes, could not pass beyond the tight junction area into the lumen. This study suggests that the pancreatic enzymes can not leak out from the glandular lumen into the intercellular spaces by dissociation of intercellular junctions even if the pancreas is stimulated by a high concentration of pancreozymin.

Animals↗
PubMed2003

Effect of glucose polymer on the intercellular junctions of cultured human peritoneal mesothelial cells.

BACKGROUND: Glucose polymer is an active osmotic agent that is increasingly used as an alternative to glucose in peritoneal dialysis fluids. It was recently reported that the duration of peritoneal dialysis can be extended by using glucose polymer in patients with poor ultrafiltration. We previously demonstrated that high glucose levels damage the intercellular junctions of cultured human peritoneal mesothelial cells (HPMC), but little is known about the influence of glucose polymer. Therefore, we investigated the effects of glucose polymer on the intercellular junctions of HPMC. METHODS: HPMC were isolated, cultured, and identified according to the modified method of Stylianou. M199 medium was supplemented with peritoneal dialysis solutions containing 7.5% glucose polymer or 1.5, 2.5, and 4.25% glucose. After 6 h, cell viability was assessed, intercellular junction proteins were examined by immunofluorescence techniques, and the concentration of transforming growth factor-beta1 in the culture supernatant was determined. RESULTS: Glucose significantly suppressed cell viability and significantly increased transforming growth factor-beta1 production when compared with control or glucose polymer cultures. Peritoneal dialysis solutions containing 4.25% glucose caused the detachment of HPMC. Immunofluorescence of intercellular junction proteins (tight junctions: ZO-1, occludin, and claudin-1; adherens junctions: beta-catenin) became weak and uneven after culture with glucose. On the other hand, glucose polymer caused little change in the immunofluorescence of these proteins when compared with control cultures. CONCLUSIONS: Glucose polymer seems to be less toxic to HPMC than glucose itself, suggesting that the glucose polymer may be better for peritoneal dialysis.

Adherens Junctions↗
PubMed1998

Structure of cardiac gap junction intercellular channels.

Gap junction proteins, termed connexins, constitute a multigene family of polytopic membrane channel proteins that have four hydrophobic transmembrane domains with the N- and C-termini located on the cytoplasmic membrane face. The principal gap junction protein in the heart, alpha 1 connexin (also designated Cx43), mediates action potential propagation between cells in order to synchronize cardiac contraction. alpha 1 connexin channels are concentrated in gap junction plaques located in the intercalated disks. The intercellular channel is formed by the docking of two hemi-channels, termed connexons, formed by a ring of six 43-kDa alpha 1 connexin subunits. Each subunit is asymmetric with an axial ratio of 4-5:1 with approximately 20 A extending into the extracellular gap approximately 50 A spanning the lipid bilayer and approximately 50 A extending into the cytoplasmic space. We have recently grown two-dimensional crystals of a recombinant C-terminal truncation mutant of alpha 1 connexin (designated alpha 1Cx263T) that are ordered to better than 7 A resolution. Projection density maps derived by electron cryocrystallography revealed that the intercellular channel is lined by six alpha-helices, and there is a second ring of six alpha-helices at the interface with the membrane lipids. These rings of alpha-helices are staggered by 30 degrees, which predicts that the two connexons in the channel are staggered by 30 degrees such that each connexin subunit in one connexon interacts with two subunits in the apposed connexon. Such a quaternary arrangement may confer stability in the docking of the connexons to form a tight electrical seal for intercellular current flow during cardiac conduction.

Amino Acid Sequence↗
PubMed2004

Localization of alkaline phosphatase and proteins related to intercellular junctions in rat hepatoma cell line McA-RH 7777.

We investigated the localization of alkaline phosphatase (ALP) and three proteins related to intercellular junctions in the McA-RH 7777 rat hepatoma cell line to determine if the formation of junctions between adjacent McA-RH 7777 cells triggers translocation of ALP from cytoplasm to the plasma membrane. Contact between adjacent McA-RH 7777 cells promotes translocation of ALP from the Golgi area of the cytoplasm to the plasma membrane, and also promotes translocation of two proteins, E-cadherin and ZO-1, related to intercellular junctions, from cytoplasm to the plasma membrane.

Adherens Junctions↗
PubMed1980

Characterization of intercellular junctions in the caudal portion of the developing neural tube of the chick embryo.

The types of intercellular junctions present within caudal levels of the chick neural tube (i.e., future lower thoracic and lumbosacral regions of the spinal cord) were determined by freeze-fracture of stage 14 to 16 embryos. Two levels of the developing neural tube were examined: the region of the neurulation overlap zone--consisting of primary neural tube dorsally and secondary neural tube ventrally--and the portion of the primary neural tube located just cranial to the overlapping region. Gap junctions were the most numerous type of intercellular junction present within the primary neural tube. These junctions were located primarily in juxtaluminal areas, near the apices of neuroepithelial cells, and sometimes also at the bases of these same cells. In addition, focal, poorly defined tight junctions occasionally occupied juxtaluminal regions of the primary neural tube. The medullary cord (i.e., the immediate precursor of the secondary neural tube) and secondary neural tube contained gap junctions exclusively. Gap junctions were first found in these areas at the lateral borders of the medullary cord, concomitant with formation of this structure, and then at the interface between the elongated, peripheral cells of the cord and the irregularly shaped and loosely arranged central cells of this structure. Finally, gap junctions were distributed radially around secondary lumina formed by cavitation. The precise spatial and temporal correlation between the appearance of gap junctions and the specific changes occurring in cellular morphology and arrangement during secondary neurulation strongly suggest that gap junctions may have a role in coordinating cellular activities during formation of both the medullary cord and the secondary neural tube.

Animals↗
PubMed1997

[Effects of diesel exhaust particle on gap junction intercellular communication].

Scrape-loading and dye transfer technique (SLDT) was used to study the effects of diesel exhaust particle (DEP) on gap junction intercellular communication (GJIC). The results demonstrated that the extract of DEP caused inhibition of gap junction intercellular communication in Balb/c 3T3 cells. It was suggested that inhibition of gap junction intercellular communication in cells may be one of the cause to induce cell transformation.

3T3 Cells↗
PubMed1989

[Electron microscopic study of intercellular junction in nasal mucosa of nasal allergy by lectin histochemistry].

To explain of the mechanism of the enhanced nasal epithelial permeability to HRP in patients with nasal allergy, the inferior turbinate mucosa was removed from 6 normal adults and 7 adults with nasal allergy. Difference of the fine structure of the intercellular junction was compared between normal mucosa and mucosa of nasal allergy by electron microscope. Staining pattern of four kinds of HRP-conjugated lectin (HRP-WGA, PNA, UEA-I and RCA-I) was also studied by electron microscope. There was no significant difference in the intercellular space of the mucosa between the normal mucosa and mucosa of nasal allergy. In the epithelial cell membrane, pattern of HRP-lectin staining was almost similar in both groups. In normal nasal epithelium, the intercellular junction consisted of junctional complex; adherent junction, desmosome and gap junction. The intercellular space was approximately 150-250 A in width. The tight junction was located beneath the luminal surface of the epithelium, and belt-like continuation connecting the adjacent cells. It was concluded that enhanced permeability to HRP in nasal allergy was not morphologic changes of the intercellular junction and component and distribution of the glycoconjugates in epithelial cellular membrane, but this may be based on functional changes.

Glycoconjugates↗
PubMed1989

Herbimycin A suppresses the reduction of gap-junctional intercellular communication induced by tumor-promoting phorbol ester in 3T3-L1 cells.

We have examined the suppressive effect of herbimycin A on the reduction of gap-junctional intercellular communication that is induced by a tumor-promoting phorbol ester in 3T3-L1 cells. Most cells in growth arrest participated in dye-coupling, as evaluated by the transfer between cells of a fluorescent dye (Lucifer Yellow CH). Treatment of cells with 0.25 microgram/ml herbimycin A slightly enhanced the dye-coupling. This enhancement required treatment for periods as long as 24 h. Addition of 100 ng/ml 12-O-tetradecanoylphorbol-13-acetate (TPA) caused a rapid reduction of dye-coupling. However, addition of TPA did not suppress dye-coupling in cells pretreated for more than 24 h with herbimycin A. Pretreatment of cells for less than 6 h with herbimycin A did not suppress the TPA-induced reduction of dye-coupling. These results suggest that herbimycin A suppresses the reduction of gap-junctional intercellular communication that is induced by TPA through enhancement of the ability of the cells to participate in gap-junctional intercellular communication.

Animals↗
PubMed2001

Effect of cadmium on gap junctional intercellular communication in primary cultures of rat renal proximal tubular cells.

Cadmium mainly accumulates in the kidney and causes renal injury. To clarify the mechanism of Cd nephrotoxicity, we investigated the effects of this element on intercellular communication through gap junction channels in primary cultures of rat renal proximal tubular cells. Sixty minutes after exposure to 100 microM Cd, dye coupling experiments showed that gap junctional intercellular communication (GJIC) was significantly inhibited. This inhibition occurred before the appearance of cytotoxicity. Intracellular calcium concentrations [Ca2+]i, which modulate the function of gap junctions, gradually increased after exposure to Cd and reached a maximum after 60 minutes. These results suggest that the inhibition of GJIC as a result of Cd exposure is related to an increase in [Ca2+]i, and that GJIC inhibition may be an indicator of nephrotoxicity.

Acetylglucosaminidase↗