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PubMed1999

Spatiotemporal development and distribution of intercellular junctions in adult rat cardiomyocytes in culture.

The mode of development of the intercalated disk (ID) is largely unknown, and the hypothesis was tested that the assembly of cell adhesion junctions may precede the formation of gap junctions (GJ) in developing ID in adult rat cardiomyocyte (ARC) in long-term culture. Immunostaining for connexin 43 (Cx43) and for cell adhesion junction proteins (N-cadherin, catenins, and desmoplakin) in single- and double-label techniques was analyzed and quantified by confocal and electron microscopy. All proteins investigated disappeared 48 hours after ARC isolation and reappeared parallel to redifferentiation of ARC. The newly formed ID, observed after 5 days, showed the presence of N-cadherin, catenins, and desmoplakin, low levels of Cx43, and absence of ultrastructurally discernible gap junctions. A progressive incorporation of Cx43 within ID was observed after 6 days, when cell adhesion junction proteins were already organized as zipper-like structures. Quantitative confocal analysis revealed a progressive augmentation of the fluorescence intensity of Cx43, associated with an increase in both the number and size of GJ, resulting in a substantial increase in the percentage of total GJ length per reassembled ID from 1.67% (day 6) to 15.58% (day 12). In the present study, we show that (1) the formation of the ID can be followed in ARC in culture and (2) the assembly of the adhering type of junction is the prerequisite for subsequent GJ formation within the ID. These findings may have clinical relevance in elaborating strategies for using myocardial grafts and for the potential restoration of GJ communication in cardiac diseases.

Age Factors↗
PubMed1995

Rearrangement of intercellular junctions and cytoskeletal proteins during rabbit myocardium development.

A direct and close association between desmosomes and intermediate-sized filaments of the keratin type exists in embryonic and in adult epithelial tissues. Cardiomyocytes are interconnected by spot-desmosomes, which are found in the intercalated disks and can be immunocytochemically detected by antibodies to desmoplakins. In this study, at the light microscopical level, we describe an interaction of keratin filaments with desmoplakins during rabbit myocardiogenesis. In the early stages (0-1 somites), desmoplakins are more abundant in the heart anlagen than in the adjacent intra- and extraembryonic mesoderm. During development of the myocardium, desmoplakin expression gradually rearranges from an apicolateral into an intercalated disk localization in later states. Keratin expression in the developing myocardium of the rabbit heart decreases with the age of the embryo. Keratin filaments are gradually lost via dot-like aggregates which colocalize with desmoplakin-positive clusters. Our results suggest a role for keratins in the developmental rearrangement of desmoplakins into the intercalated disks. A direct relation of desmin and titin reorganization to desmoplakin rearrangement, which was examined because of the dominant role of these proteins in cardiogenesis, was not found.

Animals↗
PubMed2000

Expression of beta-catenins and cadherins by follicular dendritic cells in human lymph nodes.

In lymph nodes, dendritic cells form a complex meshwork and are linked by intercellular junctions. Intercellular junctions contribute to the integrity of lymphatic follicles and can potentially be affected by malignant processes in neighbouring B cells. We examined whether transmembrane molecules that constitute "adherens junctions" are present in follicular dendritic cells of normal human lymph nodes. We found that follicular dendritic cells but not interdigitating dendritic cells or sinus lining cells expressed cadherin molecules. Follicular dendritic cells also expressed beta-catenin but not vinculin. The cadherin molecules, which were identified in situ with the use of a monoclonal pan-cadherin antibody, were not recognized by antibodies to E-cadherin, N-cadherin or P-cadherin. Intrafollicularly, cadherins were clearly colocalized with beta-catenins, in a dot-like fashion. We also detected intrafollicular expression of desmogleins and desmosomal plaque proteins. These findings indicate the presence of desmosomes within the dendritic meshwork. However, pan-cadherin reactivity was not only colocalized with desmoglein immunoreactivity that was abundantly present. Immunoprecipitation showed that pan-cadherin reactivity was absent in fractions of desmosomal plaque proteins or pan-desmogleins. We speculate that complexes of cadherins of an unknown subclass and beta-catenins form non-desmosomal intercellular junctions in the intrafollicular dendritic meshwork.

Cadherins↗
PubMed2002

[Abnormal shift of connexin 43 gap-junction protein induced by 50 Hz electromagnetic fields in Chinese hamster lung cells].

OBJECTIVE: To study the effects of extremely low frequency magnetic fields(ELF MF) on the amount and localization of connexin 43(Cx43) gap-junction protein in the Chinese hamster lung(CHL) cells, and to explore the mechanism of ELF MF suppression on gap-junctional intercellular communication(GJIC). METHODS: The cells were irradiated for 24 h with 50 Hz sinusoidal magnetic field at 0.8 mT without or with 12-O-tetrade-canoylphorbol-3-acetate(TPA), 5 ng/ml for 1 h. The localization of Cx43 proteins were performed by indirect immunofluorescence histochemical analysis and detected by confocal microscopy. The second experiment was conducted to examine the quantity of Cx43 proteins level in nuclei or cytoplasm and detected by Western blotting analysis. RESULTS: The cells exposed to TPA for 1 h displayed less bright labelled spots in the regions of intercellular junction than the normal cells. Most of Cx43 labelled spots occurred in the cytoplasm and aggregated near the nuclei. At the same time, the amount of Cx43 protein in cytoplasm were increased[(2.03 +/- 0.89) in ELF group, (2.43 +/- 0.82) in TPA group] as compared to normal control(1.04 +/- 0.17) (P < 0.01). CONCLUSION: Inhibition on GJIC function by ELF MF alone or combined with TPA may be related with the shift of Cx43 from the regions of intercellular junction to the cytoplasm.

Animals↗
PubMed2002

Effect of drugs affecting synthesis or degradation of connexin on onset or completion of ethylene glycol induced inhibition of intercellular gap junctional communication.

The role of a connexin synthesis and degradation in the onset or completion of the ethylene glycol-induced inhibition of the gap junctional intercellular communication (GJIC) in V79-4 Chinese hamster cell line was studied as a model of an interaction between the cells and a potential tumor promoter. GJIC was assessed on two levels: on the cytophysiological level - the dye coupling method, and on the immunocytochemical level - the immunolabeling of connexin43. The specific activator of connexin synthesis - Dibutyryl cAMP made the onset of the EG-induced inhibition of GJIC slower, but its effect was only temporary. On the other hand it also speeded up the re-establishment of standard values of GJIC after the removal of EG. Although the non-specific inhibitor of protein degradation via proteasomes - leupeptin increased the amount of connexin plaques on cell membranes, its effect on GJIC remained insignificant. The non-specific inhibitors of transcription - actinomycin D and translation - cycloheximide significantly inhibited the re-establishment of the standard values of GJIC after the removal of EG. The results indicate that although the storage of connexins in Golghi complex probably plays the principal role in the control of the gap junctional communication, the extensive changes in GJIC activity depend on the de novo synthesis of connexin per se.

Animals↗
PubMed1986

A-CAM: a 135-kD receptor of intercellular adherens junctions. II. Antibody-mediated modulation of junction formation.

Intercellular adherens junctions between cultured lens epithelial cells are highly Ca2+-dependent and are readily dissociated upon chelation of extracellular Ca2+ ions. Addition of Ca2+ to EGTA-treated cells results in the recovery of cell-cell junctions including the reorganization of adherens junction-specific cell adhesion molecule (A-CAM), vinculin, and actin (Volk, T., and B. Geiger, 1986, J. Cell Biol., 103:000-000). Incubation of cells during the recovery phase with Fab' fragments of anti-A-CAM specifically inhibited the re-formation of cell-cell adherens junctions. This inhibition was accompanied by remarkable changes in microfilament organization manifested by an apparent deterioration of stress fibers and the appearance of fragmented actin bundles throughout the cytoplasm. Incubation of EGTA-dissociated cells with intact divalent anti-A-CAM antibodies in normal medium had no apparent inhibitory effect on junction formation and did not affect the assembly of actin microfilament bundles. Moreover, adherens junctions formed in the presence of the divalent antibodies became essentially Ca2+-independent, suggesting that cell-cell adhesion between them was primarily mediated by the antibodies. These studies suggest that A-CAM participates in intercellular adhesion in adherens-type junctions and point to its involvement in microfilament bundle assembly.

Actin Cytoskeleton↗
PubMed1989

Novel arthropod cell junctions with restrictive intercellular 'linkers'.

The peripheral glial cells that surround the components of the avascular CNS in certain groups of primitive arthropods are characterized by unusual intercellular junctions. In the centipedes and millipedes (Myriapoda), these glial cells are associated by interconnecting filamentous 'linkers' which produce a reduction, but not an occlusion, of the intercellular cleft; these are interposed between conventional gap junctions. In replicas, the freeze-cleave images are of loosely aggregated gap junctional connection plaques, fracturing on to the extracellular membrane half leaflet (E face), together with linear alignments of intramembranous particles (IMPs) and furrows; complementary P face ridges also occur. Exogenous tracers appear unable to penetrate beyond these junction-rich glial clefts, possibly by binding to the 'linkers' or extracellular matrix between them. Peripheral glial cells in the cerebral ganglion of the horseshoe crab, Limulus, are also characterized by linear IMP arrays; in this case they primarily exhibit E face grooves and complementary ridges of P face IMPs, which also do not produce complete membrane fusion. These, too, are intimately associated with gap junctional plaques of E face particles or P face pits. These intramembranous particle rows are novel structural modifications, called here 'linker' junctions, and are quite distinct from conventional tight or septate junctions found between the outer glial cells in more highly evolved arthropods such as the insects and arachnids. They seem to represent a new category of intercellular junction.

Animals↗
PubMed2003

[The role of intercellular communication via "gap junctions" in disease].

Gap junctional intercellular communication plays an important role in the maintenance of cellular homeostasis. The flow of chemical messengers through gap junctions, gap junctional intercellular communication, is essential in processes such as electrical coupling, embryonic development and adaptive tissue response. Gap junctions are formed by connexin proteins. Mutational alterations in the connexin genes are associated with the occurrence of multiple diseases, such as peripheral neuropathy, cardiovascular disease, dermatological disease, hereditary deafness and cataract. Consequently, modulation of gap junctional intercellular communication is a potential pharmacological target. Future research, based, for example, on the recent developments in genetics, may clarify gap junction physiology. This will in turn provide promising perspectives for the development of targeted drugs.

Cardiovascular Diseases↗