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PubMed1992

Role of intercellular junctions in the passage of horseradish peroxidase across aortic endothelium.

BACKGROUND: The manner in which molecules are transported across the arterial endothelial layer has been a subject open to much interpretation and controversy. Further elucidation and clarification of these mechanisms are of primary interest. EXPERIMENTAL DESIGN: To investigate the ultrastructural features of arterial endothelial junctions and to evaluate their functional roles as a transendothelial pathway for macromolecular transport, experiments were performed on the thoracic aortae of adult male Sprague-Dawley rats by using the ultrathin serial sectioning technique and horseradish peroxidase (HRP). The aorta was perfusion-fixed with or without prior intravenous injection of HRP. RESULTS: The intercellular clefts exhibited a great deal of variety in shape, being linear, winding, interdigitated, irregular and/or dumbbell-shaped in appearance. Besides the typical 20-nm width encountered at the uniform region of intercellular clefts, local widenings (up to several hundred nm) were quite common. The arterial endothelial junctions were highly organized. Junctional elements, including tight junctions and gap junctions, were frequently present in the same intercellular cleft, even on the same plane of sectioning. Sometimes, gap junctions were found without tight junctions, but the intercellular clefts were rarely obliterated by tight junctions alone. Some intercellular clefts were not obliterated by either gap or tight junctions, and HRP was found to reach the subendothelial space by passing through these junctionless clefts. Densitometric determination of the HRP concentration profile in such junctionless clefts showed a decreasing gradient from the luminal to the abluminal front. The serial sections provided evidence that the apparently free vesicles were actually plasmalemmal membrane invaginations open to the luminal or abluminal front in the arterial endothelium. CONCLUSIONS: The present study showed that the junctionless normal endothelial clefts, in addition to the transiently open junctions surrounding mitotic cells, might provide a significant pathway in the transendothelial transport of macromolecules with the size of HRP.

Animals↗
PubMed1991

Mutagenicity and effect on gap-junctional intercellular communication of 4,4'-methylenebis(2-chloroaniline) and its oxidized metabolites.

Oxidized metabolites of 4,4'-methylenebis(2-chloroaniline) (MBOCA) were tested for direct mutagenicity in a Salmonella typhimurium assay and for effects on gap-junctional communication of WB-F344 rat liver cells. The mutagenicities of the N-hydroxy, mononitroso and o-hydroxy (ring) metabolites of MBOCA were assayed without adding activating enzyme systems, using the frame-shift sensitive strain TA98 and the base pair substitution sensitive strain TA100. The mutagenicity of the hydroxylamine was demonstrated by a linear increase in the formation of mutant colonies in both strains, with a formation of two revertants/nmol by TA98 and 21 revertants/nmol by TA100. The mononitroso metabolite showed a slight positive effect on TA100, but effects were masked by its cytotoxicity towards this strain. This metabolite was neither mutagenic nor cytotoxic to TA98. The o-hydroxy and the dinitroso metabolites were negative for mutagenicity at concentrations up to 50 and 500 micrograms/plate, respectively. The effects of parent MBOCA and N-hydroxy, mononitroso and o-hydroxy metabolites on cell-cell communication were determined by a scrape loading/fluorescent dye transfer technique. Cytotoxicity was assessed by determination of colony-forming efficiency and lactate dehydrogenase release. MBOCA itself caused an inhibition of dye transfer at concentrations of 7.5, 11.3 and 15 nmol/ml, whereas measures of cytotoxicity were not seen until 15 and 30 nmol/ml for LDH release and plating efficiency, respectively. None of the oxidized metabolites were active in inhibiting dye transfer at non-cytotoxic concentrations.

Animals↗
PubMed1976

Intercellular junctions in the Xenopus embryo prior to gastrulation.

A freeze-fracture study of Xenopus embryos at the eight-cell stage revealed the presence of tight junctions and small aggregations of 120 A diameter intramembranous particles. These aggregations consisted of up to ten particles and resembled forming gap junctions. Examination of early blastulae showed that fully developed gap junctions were present, apparently occurring very infrequently. These results support the contention that specialized junctions mediate electrical coupling during early amphibian development.

Animals↗
PubMed1986

Intercellular junctions of hyperplastic retinal pigment epithelium.

In rats with retinopathies induced by excess fluorescent light or injections of urethane, the retinal pigment epithelium (RPE) undergoes focal hyperplasia. Neither intravascularly injected horseradish peroxidase or lanthanum nitrate penetrated the sensory retina at these hyperplastic sites. Electron microscopy revealed that this was due to the persistence of intact tight junctions among a single layer of hyperplastic cells facing the sensory retina. These junctions prevented intraocularly injected microperoxidase from passing as well. Cells within the hyperplastic foci were connected only by adherent junctions that presented no permeability barrier.

Animals↗
PubMed1998

Leishmania lipophosphoglycan reduces monocyte transendothelial migration: modulation of cell adhesion molecules, intercellular junctional proteins, and chemoattractants.

We previously identified the structural requirement for the inhibitory activity of Leishmania lipophosphoglycan (LPG) to block endothelial adhesion to monocytes. Here we showed that LPG reduces transendothelial migration of monocytes. LPG pretreatment of endothelial cells (2 microM, 1 h) reduced monocyte migration across endothelial cells activated by bacterial endotoxin (LPS) or IL-1beta (60 and 46%, respectively). A fragment of LPG (i.e., repeating phosphodisaccharide (consisting of galactosyl-mannose)) and LPG coincubated with LPG-neutralizing mAb lacks inhibitory activity on monocyte migration. Pretreatment of monocytes with LPG (2 microM, 1 h) also did not affect monocyte migration through control or LPS-activated endothelial cells. FACS analysis reveals that LPG treatment blocked the LPS-mediated expression of E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 on endothelial cells and monocyte adhesion without altering the integrity of the endothelial monolayer. LPG (2 microM, 1 h) alone was capable of altering the expression and distribution of two junctional adhesion molecules, CD31 and vascular endothelium cadherin, as well as reversing the effects of LPS on these proteins. The induction of endothelial cells by LPS to transcribe and release monocyte chemoattractant protein-1 (MCP-1) was significantly reduced by LPG (40-65%). LPG treatment of nonactivated endothelial cells also suppressed by 55 to 75% the monocyte migration triggered by a MCP-1 chemoattractant gradient, and coincubation of LPG with neutralizing mAb abrogated the inhibitory activity. Together, these data point to a novel anti-inflammatory function of LPG in reducing monocyte migration across endothelial cells via a mechanism of inhibition of endothelial expression of cell adhesion molecules, modulation of intercellular junctional proteins, and synthesis of MCP-1.

Animals↗
PubMed1993

Electron microscopic study of intercellular junctions in human gastric mucosa with special reference to their relationship to gastric ulcer.

The development of gap junctions in the human gastric mucosa has been examined to see if there is any relation to gastric ulcer. Freeze fracture replicas were prepared from the endoscopic biopsy specimens of 20 patients with gastric ulcer (15 men and five women, aged 49 (13) years) and seven healthy volunteers (four men and three women, aged 41 (19) years). Large fractured areas of lateral cell membranes of surface mucous cells were observed randomly at a direct magnification of 15,000 using electron microscopy. Small gap junctions were observed between gastric surface mucous cells in all healthy volunteers. Gap junctions in the patients with gastric ulcer were significantly fewer than in the healthy volunteers. In addition, gap junctions in patients with recurrent ulcer were significantly fewer than in those with first onset ulcer. There was no obvious relationship between age and the development of gap junctions in patients with gastric ulcer or in healthy volunteers. In areas of intestinal metaplasia, gap junctions were occasionally seen between absorptive cells of the villi, but not in the lateral membranes of goblet cells. These findings suggest that loss of intercellular communication via gap junctions is associated with gastric ulcer formation.

Female↗
PubMed1981

Ultrastructural changes in mouse hepatocytes exposed to vinblastine sulfate with special reference to the intercellular junctions.

The effects of a single dose (0.5 mg) of the antimicrotubular drug vinblastine sulfate on the ultrastructure of mouse hepatocytes was studied by thin sectioning and freeze-fracturing after intravenous injection of the drug. The following cytoplasmic modifications occurred in the hepatocytes: storage of lipid droplets, heavy accumulation of autophagosomes and vacuoles with very low density lipoprotein (VLDL)-like vesicles, pathological changes in the mitochondria, and dilatation of the Golgi complexes. From 30 minutes onwards the bile canaliculi appeared altered. The tight junctions surrounding the bile canaliculi became permeable to lanthanum. This increased permeability was correlated with a disorganized arrangement of tight junctional strands and localized interruptions within the zonulae occludentes. In contrast to controls the gap junctions appeared more numerous and larger in size, exhibiting a high degree of pleomorphism. In the cytoplasm gap junctional vesicles could be observed indicating the removal of gap junctions from the surface by a process of internalization. We cannot establish whether the described changes are a direct or indirect effect of vinblastine sulfate treatment. In view of the antimicrotubular effect of vinblastine sulfate we hypothesize that normal formation of gap- and tight junctions is dependent directly or indirectly on intact microtubules.

Animals↗
PubMed1981

Intercellular junctions between femoral arterial smooth muscle cells of renal hypertensive rats.

Vascular smooth muscle from femoral arteries of hypertensive rats contract autorhythmically in vitro, whereas medial smooth muscle cells from normotensive animals are normally quiescent. This behavior suggests improved intercellular communication that permits pacemakers to control large numbers of cells. We used a transmission electron microscope to search for structural evidence of such change. In the medial arterial tissue of hypertensive rats, we found pedishaped projections extending from one cell and forming a close apposition with the smooth muscle surface of a neighboring cell. Comparable structures were not found in the normotensive controls. However, numerous other forms of close appositions were found in the tissues from the hypertensive and normotensive rats. The presence of the unique pedishaped projections in the hypertensive tissue suggest a physical means of intercellular communication permitting enhanced pacemaker influence. Perhaps these projections are formed in response to the hormonal environment seen prior to and during renal hypertension.

Animals↗