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PubMed1983

Intracellular SITS injection dye-uncouples mammalian oligodendrocytes in culture.

When the blue fluorescing dye SITS (4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid disodium salt) is injected into one of a pair of electrically and dye-coupled oligodendrocytes it does not cross the intercellular junctions but remains in the injected cell. Moreover, the fluorescent dye Lucifer Yellow CH (LY), which normally crosses these intercellular junctions after injection, does not diffuse into a SITS-injected cell. Thus, intracellular SITS injection leads to dye-uncoupling. SITS injection does not eliminate electrical-coupling.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1983

Permeability of single capillaries to intermediate-sized colored solutes.

The fiber matrix theory of capillary permeability was evaluated by measuring permeability coefficients to colored solutes with Stokes radii between 0.5 and 1.76 nm. In vivo calibration of a microscope photometer established the range of linearity for optical density measurements from a rectangular window that included the test capillary and surrounding tissue. In individually perfused capillaries of frog mesentery the following permeability coefficients, expressed as mean +/- SE X 10(5) cm/s were obtained: azure C (mol wt 277), 11.0 +/- 0.2; patent blue violet (566), 3.95 +/- 0.67; Evans blue (960), 1.15 +/- 0.23; microperoxidase (1,900), 1.13 +/- 0.31; and FITC-dextran 3 (3,400), 0.48 +/- 0.18. There is significant restriction to diffusion of all solutes larger than azure C. Fibers 0.5 nm in radius occupying 8.5% of the volume of intercellular junctions (area 2.2 X 10(-3) cm2/cm2, depth 0.6 X 10(-4) cm) account for the 22-fold range of measured permeabilities. The fiber density estimated is larger than that required to describe water flow through the junction. Negative charges on solutes larger than 0.5 nm radius may contribute to exclusion and restriction to diffusion in intercellular junctions.

Animals↗
PubMed1975

[Electron microscopic study of choroid plexus in experimentally induced hydrocephalic dog (author's transl)].

Choroid plexus in experimentally induced hydrocephalic dogs according to the Wisniewski's method was examined by an electron microscope. Epithelial cell of the choroid plexus appeared in various deformation and formed a marked dilatation of extracellular spaces between apposed two cell membranes and at the basal interdigitation. Dilatation of the extracellular space was more pronounced at the stromal side of the epithelial layer. This finding might be due to anatomical specificities of apposed epithelial cell membranes and not only indicate a disturbance of the CSF secretion. According to the dilatation of extracellular space, apposed two epithelial cell membranes separated each other, however, at sites of intercellular junctions, adjacent cell membranes remained closely apposed. The dilated extracellular space at the basal site continued to the dilated intercellular space, while, no continuity was recognized between the dilated intercellular space and ventricular lumen. These extracellular speces appeared low electron density and showed little specific structure. No particular change was recognized in organelles in the epithelial cell, except increased pinocytotic vesicles in number. Stroma of the choroid plexus appeared edematous, that was, electron density was low and a few cellular and stromal elements were found. Capillary vessels showed almost normal structure. In hydrocephalic dogs also in normal one, Lanthanum infused into lateral ventricle precipitated on the surface of microvilli of choroid plexus epithelial cell. The Lanthanum, entered through ventricular end of intercellular space, was blocked to penetrate beyond the intercellular junction (zonula occludens) and any bit of the tracer was not found in the dilated extracellular space. The tracer was found neither in epithelial cell nor in stroma. These findings of tracer-study may indicate that the CSF absorption through the choroid plexus is not increased in chronic hydrocephalus. Consequently, the ultrastructural changes of the choroid plexus in chronic hydrocephalus, that is, enlarged extracellualr space, increased pinocytotic vesicles and edematous stroma, are thought to suggest a disturbance of CSF secretion from the choroid plexus.

Animals↗
PubMed1994

Intercellular interactions in PC12 cells overexpressing beta/A4 amyloid.

The amyloid precursor protein (APP) is an integral membrane component of eukaryotic cells. A variety of research approaches have addressed the contribution of the beta amyloid peptide region of the APP to neuritic plaque structure and formation in the Alzheimer disease brain as well as the relationship between beta amyloid accumulation and the occurrence of dementia. However, there is limited information available concerning the cellular consequences of amyloid deposition. The present studies were undertaken to investigate the relationship between beta amyloid and intercellular junctions. Transfected PC12 cell lines, that overexpress the beta amyloid peptide, exhibit structural and functional alterations at the cell surface and tend to form aggregates more readily than normal control cells. Intermediate junctions were the most common intercellular interactions of both normal and transfected cells. However, the control and transfected cells differed since areas of continuous and extensive junctions were readily seen in transfected cells and infrequently seen in control cells. The data suggest that excess accumulation of beta amyloid is associated with the junctional apparatus and may be related to increased intercellular adhesion.

Actins↗
PubMed1985

Sialographic damage in rat submandibular gland.

The damage caused to rat submandibular glands by intraductal injection was examined. When a small volume of isotonic saline was injected, even if salivation was not influenced, salivary composition was greatly affected because the intercellular junctions of the duct cells were damaged. Intraductal injections of hyperosmotic solutions or highly viscous liquids were more effective in damaging intercellular junctions. When interpreting the significance of a salivary composition in clinical diagnosis, it is necessary to consider the sialographic damage which might influence the salivary composition.

Animals↗
PubMed1986

Distribution of cell surface charges on mesothelium and lymphatic endothelium.

The distribution of anionic sites on the luminal surfaces of the peritoneal mesothelium and lymphatic endothelium was investigated by injecting cationized ferritin (CF) intraperitoneally. After washing with phosphate-buffered saline, the diaphragm was fixed and processed for electron microscopy. CF label occurred in discontinuous patches along the mesothelial surface. Microvilli were heavily marked and often closely applied to the mesothelial surface. The intercellular cleft was also heavily labeled. The luminal aspect of the lymphatic endothelium was more extensively labeled, with the marker occurring in long discontinuous dense bands. The clefts of lymphatic endothelial intercellular junctions were extensively labeled especially along regions where cells were loosely apposed. The existence of a high density of anionic sites on membranes at the intercellular junctions of both mesothelial and lymphatic endothelial cells represent a salient feature which is very different from binding in blood capillary endothelium. The presence of a high density of anionic sites along the intercellular clefts of adjacent cells may play a role in the rapid movement of small solutes and molecules from interstitial spaces into the lymphatic lumen.

Animals↗
PubMed1976

Gap junctions between human meningioma cells maintained in organ culture.

Intercellular junctions were commonly observed in a human syncitial meningioma maintained in organ culture for up to 44 days in vitro (DIV) using gelatin sponge foam matrices. The junctions were identified as one of three types: desmosomes; tight junctions; or gap junctions. Of the three types, gap junctions were frequently encountered and showed preservation of their characteristic ladder-like substructure. The results suggest that organ culture provides an environment that may facilitate correlation of the structure and function of gap junctions between coupled human meningioma cells.

Brain Neoplasms↗
PubMed1975

Junctions in the meninges and marginal glia.

The meninges of various mammals were prepared for examination with the electronmicroscope by thin sectioning or freeze-fracturing. Particular attention was given to the distribution of tight junctions in order to determine the basis for the meningeal barrier between the blood circulating in dural vessels and the cerebrospinal fluid in the subarachnoid space. While some dural blood vessels are fenestrated, those in the subarachnoid space are not and their component endothelial cells are joined by an extensive system of tight junctions. An extensive and continuous system of tight junctions was also found in a layer of specialized cells at the border of the arachnoid with the dura. This arachnoid barrier layer is apparently the only basis of the meningeal barrier because often cellular layers in the dura and arachnoid lack tight junctions although they are linked by gap junctions and desmosomes. In particular, tight junctions are lacking at the border of the "subdural space" which is actually a fascial plane within the dura. Tight junctions are also lacking between astrocytes at the surface of the brain but these cells are linked by gap junctions and a new type of intercellular junction. The distribution of these junctions, as well as assemblies of intramembranous particles at the astrocytic border, raises the question whether this layer might have a role in the exchange of certain substances between the brain and cerebrospinal fluid.

Animals↗
PubMed1985

The distribution of the main intrinsic membrane polypeptide in ocular lens.

The Main Intrinsic Polypeptide (MIP) of the ocular lens fiber cell plasma membrane was immunocytochemically localized at the ultrastructural level on ultrathin frozen sections of rat lens, and on extracted, gradient-purified bovine lens membranes. The results indicate that both the junctional and non-junctional membrane domains of the cortical lens fiber cell are MIP immunoreactive. Frozen thin section immunocytochemistry of the lens epithelium and hepatocytes, also using anti-MIP antibodies, revealed that these cells, and their intercellular junctions, are not MIP-immunoreactive. From these findings we conclude that 1) MIP, a putative fiber cell junctional protein, is present throughout the plasma membrane of the lens fiber cell, and is not confined to the fiber cell junctional domain, 2) MIP is not a detectable component of the lens epithelial cell membrane, or its intercellular junctions, 3) MIP is not detectable in gap junctions of hepatocytes.

Animals↗
PubMed2004

Electron microscopy of degenerative changes in the chick basilar papilla after gentamicin exposure.

We present a sequential study of the substructural alterations in the chick basilar papilla at the earliest signs of hair cell degeneration. Three-day posthatch chicks received a single injection of gentamicin (300 mg/kg) and were killed at 6, 8, 12, 15, 18, 21, and 24 hours after the injection. The basilar papillae were studied by conventional transmission electron microscopy. Examination was limited to the basal region, where all hair cells are eliminated by this treatment. As early as 8 hours and clearly by 12 hours, altered fine structure was seen in hair cells. Changes included rounding and swelling of the hair cells, condensation of nuclear chromatin, dissolution of ribosomes, dilatation of the mitochondria, and accumulation of inclusion bodies and lysosomes. By 15-18 hours, lysosomes increased and became denser, afferent terminals appeared swollen, and the first cell extrusion was seen. Efferents were unaffected, and supporting cells, though having inclusion bodies now, retained normal intercellular junctions. By 21-24 hours, large regions of complete hair cell loss were composed of expanded supporting cell processes with normal-appearing intercellular junctions and portions of extruded hair cells, partially attached to the supporting cell surface. These observations demonstrate that auditory hair cells undergo a rapid and controlled process of hair cell extrusion that allows preservation of the reticular lamina and minimal contamination of surrounding structures by intracytoplasmic contents of the damaged hair cells.

Animals↗
PubMed2005

Histone deacetylase inhibitors induce G2-checkpoint arrest and apoptosis in cisplatinum-resistant ovarian cancer cells associated with overexpression of the Bcl-2-related protein Bad.

Trichostatin A produces predominantly G(1) cell-cycle blockade and differentiation of the cisplatinum-sensitive A2780 ovarian cancer cell line. Given the propensity of ovarian tumors to become resistant to cisplatinum, often leading to cross-resistance to other agents, we have extended these observations by examining how the emergence of resistant phenotypes in A2780 cells affects the actions of histone deacetylase (HDAC) inhibitors. Trichostatin A exposure (100 ng/mL, 24 hours) induced ultrastructural differentiation of the "intrinsically" cisplatinum-resistant A2780-9M subline, with the reappearance of intercellular junctions and lumina containing primitive microvilli. Similar trichostatin A exposure in the acquired resistance A2780CP cells produced minimal differentiation consisting of occasional weak intercellular junctions. Independent of the differences in trichostatin A-induced differentiation, in both resistant sublines trichostatin A produced a similar reduction in cell viability, by >90%, within 5 days of treatment. Diminished viability in both A2780-9M and CP cells was associated with the absence of cell cycle arrest in G1, resulting in predominant G2-checkpoint arrest accompanied by a 10- to 20-fold increase in Annexin V binding and the reemergence of apoptosis. Similar cell cycle arrests and apoptosis were also observed using other HDAC inhibitors and in other resistant ovarian cancer cell lines (OVCAR-3 and SK-OV-3). Trichostatin A-induced apoptosis in resistant cells is in sharp contrast to its effects on the parental cisplatinum-sensitive A2780 and normal MRC-5 fibroblast cell lines (predominant cycle arrest in G1 with no detectable apoptosis). Western immunoblot analysis indicated trichostatin A triggers apoptosis in resistant ovarian cancer cells via p53-independent activation of the intrinsic "mitochondrial" pathway, commensurate with induction of the Bcl-2-related protein Bad. These results suggest cisplatinum resistance alters the effects of HDAC inhibition through a shift in cell cycle arrest from the G1 to the G2 checkpoint and reactivation of the intrinsic mitochondrial apoptotic cascade.

Annexin A5↗
PubMed1990

Integrity of the dissociated adult cardiac myocyte: gap junction tearing and the mechanism of plasma membrane resealing.

Dissociation of adult cardiac myocytes by collagenase perfusion techniques requires separation of the junctional contacts that link the cells physically, electrically and metabolically in the intact heart. Gap junctions, one of three types of intercellular junction present at the cardiac intercalated disc, are not split into their component membranes when myocytes are dissociated; they are ripped from the plasma membrane of one cell, to be retained by its neighbour. Partitioning of junctions in this way might be expected to constitute a serious threat to the ionic integrity of dissociated myocytes, but in practice, high yields of functionally intact cells, suitable for experimental studies, are routinely obtained. To explain this apparent paradox, repair mechanisms, operating to seal the membrane lesions caused by gap junction tearing, have been hypothesized, but evidence for their existence has previously been lacking. Using freeze-fracture electron microscopy, the present study identifies repair sites as smooth membrane domains that are continuous with the neighbouring plasma membrane, thus forming intact seals. That these structures are not chemically-induced artefacts is demonstrated by their presence in myocytes that were frozen directly from the living state. Subsarcolemmal vesicle clusters, detected in thin sections and freeze-fracture replicas, are associated with the smooth sealing domains. These structures may represent either rounded-up fragments of mechanically disrupted membrane or structures concerned with the synthesis of new lipid. From their freeze-fracture morphology, the sealing domains appear to be lipid-rich and protein-poor. Cytochemical studies using Ruthenium Red, cationized ferritin and lectins show in addition that they have a lower content of negatively-charged membrane components than the neighbouring plasma membrane, and that the carbohydrate residues normally associated with plasma membrane glycolipids and glycoproteins are absent.

Animals↗
PubMed1994

Hormonal regulation of connexin 43 expression and gap junctional communication in human osteoblastic cells.

We have recently shown that connexin 43 (Cx43), a major gap junction protein in osteoblasts, is expressed with an increase in cell density (CHIBA, H. et al. (1993). Cell Struc. Funct., 18: 419-426). In the present study, we examined what kinds of hormones and cytokines regulate the gap junction protein in osteoblastic cells, using a human osteoblastic cell line (SV-HFO) after reaching a confluent density to avoid influence of cell proliferation. Either retinoic acid (RA) or transforming growth factor-beta 1 (TGF-beta 1) induced the Cx43 expression of SV-HFO cells, as revealed by Northern blot analysis and immunocytochemistry. These modulators also increased gap junctional intercellular communication, in terms of the extent of dye transfer. On the other hand, 1 alpha, 25-dihydroxyvitamin D3 did not influence the Cx43 expression and gap junctional intercellular communication of the cells. These results suggest that RA and TGF-beta might maintain bone tissue as an organized tissue in vivo by increasing intercellular communication of osteoblastic cells.

Calcitriol↗
PubMed2005

Expression of tight and gap junctional proteins in the perineurial window model of the rat sciatic nerve.

Limited perineurial injury, known as a perineurial window, can lead to neuropathic pain. This article hypothesizes that the recovery of the perineurium is associated with the intercellular junctional proteins. It analyzes the expressions of occludin, ZO-1, and connexin 43 by immunoconfocal microscopy. Seven days after injury, immunoreactivities for occludin and ZO-1 were observed, although there was no connexin 43 detected. Then, 21 days after injury, immunoreactivity for connexin 43 were observed. These results indicate that recovery of the perineurium is associated with the intercellular junctional proteins and that the recovery of gap junctions is delayed compared with that of tight junctions.

Animals↗
PubMed1992

Electrical coupling between cells of the insect Aedes albopictus.

1. Cell pairs of an insect cell line (Aedes albopictus, clone C6/36) were used to study the electrical properties of intercellular junctions. A double voltage-clamp approach was adopted to control the voltage gradient between the cells and measure the intracellular current flow. 2. Determinations of junctional conductance (gj) revealed two types of intercellular contacts, gap junctions and cytoplasmic bridges. Identification occurred by means of functional criteria, i.e. the dependency of gj on (i) junctional membrane potential, (ii) non-junctional membrane potential, and (iii) heptanol. 3. In cell pairs with putative gap junctions, gj was dependent on the junctional membrane potential (Vj). When determined at the beginning of voltage pulses, gj was insensitive to Vj; when determined at the end of 15 s pulses, it depended on Vj in a bell-shaped manner (70% decrease for a change in Vj of +/- 75 mV). 4. These cell pairs also showed a dependency of gj on the non-junctional membrane potential (Vm). When determined immediately after changing the non-junctional membrane potential in both cells, gj was not affected by Vm; when determined 30 s later, gj was modified by Vm in a S-shaped fashion (100% decrease when Vm was depolarized to +50 mV). 5. Exposure to 3 mM-heptanol gave rise to complete and reversible block of gj in cell pairs with putative gap junctions. 6. Cell pairs susceptible to uncoupling by heptanol revealed junctional currents indicative of the operation of gap junction channels. The single-channel conductance, determined at a Vm of -50 to -70 mV, was 133 pS. 7. In the case of putative cytoplasmic bridges, gj was insensitive to the junctional and non-junctional membrane potential. In addition, it was not affected by 3 mM-heptanol. 8. While most cell pairs showed functional properties characteristic of gap junctions or cytoplasmic bridges, few cell pairs exhibited junctional currents compatible with the co-existence of both junctional structures.

Aedes↗
PubMed1986

Microinjection of glycosaminoglycan-degrading enzymes in the chicken blastoderm. An ultrastructural study.

The relationship between the presence of glycosaminoglycans (GAGs) and the morphology of the middle layer or mesoblast was examined by performing transmission electron microscopy of chicken blastoderms microinjected with GAG-degrading enzymes. The controls included microinjections with saline or trypsin, as well as solid-phase assays for proteolytic activity in commercially available GAG-degrading preparations. The results indicate that, in normal as well as in saline-injected blastoderms, middle-layer cells are rounded or cuboidal in shape, and are linked to each other by small intercellular junctions in the primitive-streak region. As they migrate laterally along the basal lamina, they appear as typical mesenchymal cells, being separated by large intercellular spaces and covered by cell processes. The removal of hyaluronate (by the microinjection of hyaluronidases) led to compaction of the middle-layer cells in the area lateral to the primitive streak. These cells lost their mesenchymal aspect and retracted their processes, and intercellular junctions were observed. The presence of proteolytic activity in the enzyme preparations did not interfere with the results. On the basis of the results obtained using this microinjection technique, we were able to confirm at the ultrastructural level that hyaluronate, due to its space-creating properties, promotes the detachment of ingressed primitive-streak cells and preserves the mesenchymal aspect of the middle layer during the lateral migration of single cells along the basal lamina. Whether the presence of hyaluronate is necessary to allow positioning of the mesoblast could not be inferred using our experimental procedure. We present evidence that this molecule, as well as having physicochemical properties, is also involved in the modulation of tissue interactions during gastrulation.

Animals↗
PubMed2002

Ciliary neurotrophic factor (CNTF) in combination with its soluble receptor (CNTFRalpha) increases connexin43 expression and suppresses growth of C6 glioma cells.

The loss of gap junctional intercellular communication has been proposedas playing a major role in the process of carcinogenesis. Most neoplastic cells, including C6 gliomas, express less connexins and have fewer gap junctions, reduced gap junctional intercellular communication, and increased growth rates compared with their nonneoplastic counterparts. The purpose of this study was to determine whether ciliary neurotrophic factor (CNTF) can be used to increase endogenous connexin43 levels, increase intercellular coupling, and retard the growth rate of C6 glioma cells. C6 cells were grown in serum-reduced medium (1% serum) and exposed to the following agents: vehicle (PBS), CNTF (20 ng/ml), CNTF soluble receptor (CNTFRalpha; 200 ng/ml), or Complex (CNTF + CNTFRalpha). Reverse transcription-PCR analysis indicated that C6 cells express CNTF mRNA but not CNTFRalpha mRNA. When cells were exposed to the above agents, only Complex caused an up-regulation of connexin43 protein (based on immunocytochemical and immunoblot analysis). Furthermore, Complex increased gap junctional coupling in C6 cells as noted by the passage of the gap junction permeable dye calcein. Finally, it was demonstrated that Complex-treatment reduces the growth rate of C6 cells compared with all of the other agents tested. Taken together, this study has demonstrated that CNTF in combination with its soluble receptor can increase connexin43 expression, increase gap junctional coupling, and reduce the in vitro proliferation of C6 glioma cells.

Animals↗