Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intercellular Junctions”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources
PubMed2000

Hematopoiesis: Gap Junction Intercellular Communication is Likely to be Involved in Regulation of Stroma-dependent Proliferation of Hemopoietic Stem Cells.

The 80-100 fold increased immunohistological expression of the Gap Junction (GJ) protein Connexin-43 in murine bone marrow during the neonatal period and directly following cytoreductive treatment of adult mice suggests that the regulation of stem cell proliferation may involve GJ Intercellular Communication (GJIC). Using a series of stromal cell lines from foetal liver and neonatal bone marrow we observed that the percentage of cells with GJIC, as indicated by dye-coupling using microinjection of lucifer yellow, correlated with the stromal support for late appearing clones formed by primitive stem cells (CAFC week 3-5). In order to functionally block all GJIC between mutual stromal cells and stromal cells and hemopoietic cells, in long-term stroma-supported flask (LTC) and CAFC cultures, the lipophilic compounds amphotericin-B (AB), nystatin, alpha-glycyrrhetinic acid, tetraphenylboron, dipicrylamine and arachidonic acid were tested for their effect on GJIC and CAFC support. Only AB and nystatin, which induced complete and prolonged GJIC blockade, were able to dramatically inhibit cobblestone area (CA) formation and CFU-C generation in LTC. This inhibition could be fully abrogated by withdrawing AB within the first 2 weeks of culture. Low AB concentrations stimulated CA formation. The AB-mediated inhibition of hemopoiesis probably involved direct stromal contact with stem cells because a) AB did not inhibit CFU-C generation when stem cells were cultured in trans-well inserts above the stroma; b) conditioned media from AB-containing or normal LTC did not inhibit colony formation by normal cells in semi-solid, non-stromal cultures, and c) AB did not inhibit colony formation by bone marrow cells in semi-solid culture nor did it inhibit growth or maintenance of stromal cells. In addition, The inhibition of hemopoiesis by AB could also not be explained by changes in the amount of cytokine and chemokine transcripts, including TGF-b1, in AB-blocked stromal cells. Our findings support the involvement of GJIC in stroma-dependent regulation of hemopoietic stem cell proliferation.

Journal Article↗
PubMed2002

Antiviral agents alter ability of HSV-2 to disrupt gap junctional intercellular communication between mammalian cells in vitro.

In cultured mammalian cells (Vero), different antiviral agents change to differing degrees the ability of HSV2 to down-regulate gap junctions, each agent having a specific effect. Measured by intracellular electrodes, control cell populations showed 49-51% coupling, uninfected populations treated with acyclovir or SDS averaged 43-51% coupling while populations infected with HSV2 had coupling reduced to 8%. The antiviral agent acyclovir (1 microg/ml), which suppresses viral replication, failed to prevent this down regulation (final coupling ratio of 11%). A plant extract (250 microg/ml) from Pilostigma thonningii offered slightly more protection (final coupling ratio of 22%), while sodium dodecyl sulfate (SDS) (50 microM) afforded nearly complete protection (final coupling ratio of 40%). With SDS there was an initial down regulation to only 16% coupling by 3 h post infection, followed by a recovery of intercellular communication to near control levels by 24 h. While SDS was originally believed to alter the viral coat and prevent entry into the cell, our data are in agreement with recent studies which indicate that SDS treated viruses can enter into host cells, but in a severely diminished condition. Our data also suggest that the gap junction antagonist is brought into the cells as part of the entering virus.

Acyclovir↗
PubMed1989

Junctional intercellular communication is cooperatively inhibited by oncogenes in transformation.

We examined the actions of the cellular src (c-src) and adenovirus E1A genes on junctional cell-to-cell communication. Neither gene causes complete transformation of NIH3T3 cells on its own, but the two do so in conjunction with one another. This cooperation goes hand in hand with summation of the actions of the two genes on junctional communication: junctional permeability is reduced when the cells are transfected with either gene; it is reduced significantly more when they are transfected with both. This cooperative loss of communication approaches the noncooperative loss induced by the viral src gene (v-src), chimeric c-src/v-src, or Tyr527-mutant c-src--genes that cause transformation on their own. This provides a rationale for the hitherto unexplained complementation of the two oncogenes in carcinogenesis; it is the expected behavior if the loss of communication is causal in the decontrol of growth in transformation.

Adenovirus Early Proteins↗
PubMed2001

Inhibition of gap junctional intercellular communication in rat liver epithelial cells with transforming RNA.

Previous studies indicated that transforming RNA, derived from the 3' half of the U5 small nuclear RNA first stem structure, suppressed the secretory protein translation in vitro. Gap junctions facilitate homeostatic control of cell growth and differentiation and their dysfunction has been correlated with carcinogenesis. Here, we reported that transforming RNA directly suppressed the gap junction protein, connexin 43, translation and thereby inhibited functional gap junction function in rat epithelial cells. Together with previous data, this implies that altered expression of transforming RNA itself is a potential mechanism in inhibiting gap junction function during carcinogenesis.

Animals↗
PubMed1999

Plectin is concentrated at intercellular junctions and at the nuclear surface in morphologically differentiated rat Sertoli cells.

Intermediate filaments in Sertoli cells have a well-defined pattern of distribution. They form a basally situated perinuclear network from which filaments extend peripherally to adhesion plaques at the plasma membrane and to sites of codistribution with other major elements of the cytoskeleton, particularly with microtubules. Although the general pattern of intermediate filament distribution is known, the molecular components involved with linking the filaments to organelles and attachment plaques in these cells have not been identified. One candidate for such a linking element is plectin. In this study we test for the presence of, and determine the distribution of, plectin in Sertoli cells of the rat testis. Fixed frozen sections and fixed epithelial fragments of rat testis were probed for plectin and vimentin using antibodies. Tissue was evaluated using standard fluorescence microscopy and confocal microscopy. Plectin in Sertoli cells was concentrated in a narrow zone surrounding the nucleus, and at focal sites, presumably desmosome-like plaques, at interfaces with adjacent cells. Plectin was also concentrated at sites where intermediate filament bundles project into specialized actin-filament containing plaques at sites of attachment to elongate spermatids. Plectin in Sertoli cells is concentrated at the nuclear surface and in junction plaques associated with the plasma membrane. The pattern of distribution is consistent with plectin being involved with linking intermediate filaments centrally (basally) to the nucleus and peripherally to intercellular attachment sites.

Animals↗
PubMed2004

Glucagon increases gap junctional intercellular communication via cAMP in the isolated perfused rat liver.

The effects of glucagon on the subacinar distribution of hepatic transmembrane potentials were studied in the perfused fasted rat liver. The livers were perfused with a Krebs-Henseleit buffer, and membrane potentials of matched periportal and pericentral hepatocytes were determined using glass microelectrodes. Lactate- and pyruvate-induced glucose production and O2 uptake were potentiated by 10(-8) M glucagon. Twenty-five micromoles 8-bromoadenosine 3',5'cyclic monophosphate (8-BrcAMP) exhibited stimulatory effects similar, in terms of glucose production and O2 uptake to those of glucagon. Octanol (0.1 and 0.5 mM) had no effect on glucose production but reversibly increased O2 uptake by 16% to 30% over all experiments. Under basal conditions (no exogenous substrate) hepatocyte membrane potentials averaged approximately -27 mV, and no gradients were found between periportal and pericentral hepatocytes. Addition of lactate and pyruvate produced hyperpolarization in all hepatocytes. However, there was a small but statistically significant gradient produced across the hepatic acinus in membrane potential, i.e., the hyperpolarization was higher in the periportal region compared with the pericentral region. Glucagon and 8-BrcAMP induced marked hyperpolarization in periportal and pericentral hepatocytes with no gradients across the acinus. Although no changes were found under basal and lactate plus pyruvate, 0.5 mM octanol induced heterogeneity of membrane potential during glucagon and 8-BrcAMP stimulation. Our findings suggest that glucagon-induced homogeneity of membrane potential may be mediated by increased gap junctional coupling. In addition, cAMP may be responsible for the increase in the intercellular communication during glucagon stimulation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Breast cancer metastatic potential correlates with a breakdown in homospecific and heterospecific gap junctional intercellular communication.

Breast cancer progresses toward increasingly malignant behavior in tumorigenic and metastatic stages. In the series of events in the metastatic stage, tumor cells leave the primary tumor in breast and travel to distant sites where they establish secondary tumors, or metastases. In this report, we demonstrate that cell-cell communication via gap junctions is restored in the metastatic human breast carcinoma cell line MDA-MB-435 when it is transfected with breast metastasis suppressor 1 (BRMS1) cDNA. Furthermore, the expression profile of connexins (Cxs), the protein subunits of gap junctions, changes. Specifically, the expression of BRMS1 in MDA-MB-435 cells increases Cx43 expression and reduces Cx32 expression, resulting in a gap junction phenotype more similar to normal breast tissue. Taken together, these results suggest that gap junctional communication and the Cx expression profile may contribute to the metastatic potential of these breast cancer cells.

Breast Neoplasms↗
PubMed1995

Possible anti-tumour-promoting activity of components in Japanese soybean fermented food, Natto: effect on gap junctional intercellular communication.

In order to detect any protective agent against tumor formation, we examined the anti-tumor-promoting effect of a Japanese traditional soybean fermented food, Natto. Dye transfer was employed as an assay method. When fluorescent dye was microinjected into cultured BALB/3T3 cells, the dye was transformed into the neighboring cells through the gap junction. This dye transfer was blocked by the treatment with the tumor promoters 12-O-tetra-decanoylphorbol-13-acetate (TPA), a high concentration of NaCl and lithocholic acid (LCA). This reduction of the dye transfer by TPA treatment was not observed when the cells were pretreated with retinoic acid, an anti-tumor promoter. Thus, the recovery of the dye transfer in TPA-treated BALB/3T3 cells was proven to ge a good indicator for detecting some possible anti-tumor promoters. After extraction and fractionation of Natto, we obtained an active fraction (H1) which showed recovery of the dye transfer in TPA-treated cells. The fraction contained straight-chain saturated hydrocarbons. A comparison of the fraction and the authentic samples by GC analysis suggests that the H1 fraction contained straight-chain saturated hydrocarbons from around C30 to C32. Among these hydrocarbons, hentriacontane (C31) was found at the highest concentrations, and was shown to have the highest activity. Hentriacontane at a very low concentration of 0.65 ng/ml was shown to recover the dye transfer inhibited by the treatment with TPA as well as with NaCl and LCA.

3T3 Cells↗
PubMed2001

HSV-2 disrupts gap junctional intercellular communication between mammalian cells in vitro.

Infection by herpes simplex virus-2 (HSV-2) disrupts both dye and electrical coupling in Vero (African green monkey kidney) cell cultures. Vero cells in vitro were iontophoretically injected with the fluorescent dye Lucifer yellow CH, the spread of which revealed that cells throughout the confluent sheet shared open gap junctions. However, 24 h after infection with the virus (but before cells became rounded), dye always remained only within the target cell. Intracellular electrophysiological measurements of ionic coupling revealed a 0.4 coupling coefficient for adjacent cells in uninfected control cultures. By 3 h following infection significant down-regulation of gap junctions had begun, preceding by many hours any signs of infection visible with the light microscope. Measurements between adjacent cells 3 h post-infection, a period when HSV-2 gene expression is known to be at a maximum, yielded an average coupling coefficient of 0.35. By 6 h post-infection (a period of known viral DNA replication) average coupling coefficient for adjacent cells was 0.25, while by 24 h post-infection the average fill still further to <0.08. A coupling coefficient of <0.08 suggests that infection by HSV-2 completely disabled the gap junctions.

Animals↗
PubMedDate not supplied

Gap junction intercellular communication in gliomas is inversely related to cell motility.

Gliomas are lethal because of local invasion into brain parenchyma. Glioma cells were isolated from different regions (white matter, gray matter and tumor core) of a glioma-bearing dog brain. Individual clonal cell lines were established from each area, and characterized for growth, migration and gap junctions. The regional clonal cell lines differed in rates and preferred substrate for migration. Cell lines generated from invaded white matter showed stimulated migration on collagen and variable migration on merosin, whereas migration of cell lines derived from invaded gray matter showed the reciprocal responses: stimulation on merosin and inhibition on collagen. Gap junctional communication showed significant degrees of variation between the different clones. A direct inverse relationship between the number of cells demonstrating gap junctional communication and migration rate of cells away from multicellular spheroids was evident. Glioma cells which have a reduced capacity to connect to each other have an accelerated migration rate onto autologous, glioma-derived matrix. These results suggest that invasive glioma cells suppress autologous cell-to-cell cohesion, partly evident as reduced formation of gap junctions. In addition, glioma cells were stimulated to migrate in a dose-dependant manner in response to epidermal growth factor (EGF) coincident with the reduction of Cx43 levels and increased serine phosphorylation. We speculate that in order for glioma cells to invade locally into brain parenchyma they must first detach from neighboring cells ("let go...let's go" paradigm of invasion).

Animals↗
PubMed1986

[Ultrastructural study of the intercellular junction and lanthanum penetration in the mouse blastocyst].

Cell junctions in mouse blastocyst were ultrastructurally investigated with or without lanthanum tracer. Tight junctions, gap junctions and desmosomes were observed in the trophectoderm. The tight junction was located near the zona pellucida in all trophoblast interspaces, whereas the gap junction and the desmosome, which were infrequently observed, were localized far from the zona pellucida. However, the desmosomes in the trophectoderm of the expanded blastocyst after culture increased in number and came to be located near the zona pellucida. The trophoblast layer excluded lanthanum whose invasion was interrupted by the tight junction. There were a few intermediate junctions in the interspace between the trophoblast and the inner cell mass cell as well as between the inner cell mass cells. These findings indicate that a substances whose molecular weight exceeds that of lanthanum (138.9) may not flow into the blastocyst through the intercellular space. Moreover, it is speculated that the intercellular connection is strengthened during the expansion of the blastocyst.

Animals↗