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Junctional Complexes (junctional + complex)
Selected AbstractsMicroscopic structure of the sperm storage tubules in the polygynandrous alpine accentor, Prunella collaris (Aves)ACTA ZOOLOGICA, Issue 4 2001Akira Chiba Abstract We describe the microscopic structure of the sperm storage tubules (SSTs) of the polygynandrous alpine accentor, Prunella collaris. The SSTs were found at the utero-vaginal junction of the oviduct and were composed of a single layer of columnar epithelium. The cells of the tubule proper were non-ciliated and had a round or oval nucleus in their basal portion. Their cytoplasm was finely or coarsely vacuolated due to lipid inclusions. Under the electron microscope, the epithelial cells exhibited a number of mitochondria, Golgi bodies, occasional lysosome-like dense bodies, granular endoplasmic reticula, junctional complex, and tonofilaments. The apical margin of the cells was fringed with numerous microvilli. The epithelial lining of the SSTs was devoid of mucous cells, but showed occasional infiltration of lymphoid cells. No contractile elements were found in association with the SSTs, but a close apposition of unmyelinated nerve fibres to the basal part of the SST cells was recognized. Intraluminal sperm were arranged in bundles, and their heads were orientated towards the distal portion of the SSTs. Evidence for engulfment of sperm by the SST cells was obtained for the first time. A sign of atrophy or regression of the SSTs was found in one specimen. [source] Hyperosmotic mannitol induces Src kinase-dependent phosphorylation of ,-catenin in cerebral endothelial cellsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2005Attila Farkas Abstract Mannitol, which is a cell-impermeable and nontoxic polyalcohol, has been shown to be a useful tool for reversible opening of the blood,brain barrier (BBB). Despite successful clinical trials, the molecular mechanism of the mannitol-induced changes in cerebral endothelial cells (CECs) are poorly understood. For our experiments, we used CECs in culture, which were treated with different, clinically relevant concentrations of mannitol. We found that mannitol induced a rapid, concentration-dependent, and reversible tyrosine phosphorylation of a broad range of proteins between 50 and 190 kDa. One of the targets of tyrosine phosphorylation turned out to be the adherens junction protein ,-catenin. Phosphorylation of ,-catenin on tyrosine residues caused its subcellular redistribution and its dissociation from cadherin and ,-catenin as shown by coimmunoprecipitation studies. All these effects could be inhibited by the Src kinase inhibitor PP-1 but not by the Erk inhibitor U0126, the Rho kinase inhibitor Y27632, or the calcium channel blocker verapamil. Because ,-catenin is a key component of the junctional complex, its Src-mediated phpsphorylation may play an important role in the mannitol induced reversible opening of the BBB. © 2005 Wiley-Liss, Inc. [source] Involvement of integrin-induced activation of protein kinase C in the formation of adherens junctionsGENES TO CELLS, Issue 5 2007Misa Ozaki In epithelial cells, tight junctions (TJs) and adherens junctions (AJs) form junctional complexes. At AJs, cadherins and nectins are the major cell-cell adhesion molecules. Nectins first form cell,cell adhesions and then recruit cadherins to the nectin-based cell,cell adhesion sites to form AJs in coordination with the activation of integrin ,v,3, followed by the formation of TJs. We previously demonstrated that when MDCK cells precultured at a low Ca2+ concentration were treated with the protein kinase C (PKC) activator 12- O -tetradecanoyl-phorbol-13-acetate (TPA), incomplete AJs and a TJ-like structure were achieved. However, it remains unknown how PKC is activated and how it regulates the formation of cell,cell junctions. When MDCK cells precultured at a low Ca2+ concentration were treated with TPA, incomplete AJs were formed without the activation of integrin ,v,3. Treatment of cells with TPA also enhanced the phosphorylation of FAK, which transmits the outside-in signal of integrin and plays a role in the nectin-induced formation of AJs. In addition, inhibition of PKC suppressed the formation of AJs. These results indicate that the activation of PKC functions downstream of integrin ,v,3 and upstream of FAK, and is important for the nectin-induced formation of AJs. [source] Pigment epithelium-derived factor supports normal Müller cell development and glutamine synthetase expression after removal of the retinal pigment epitheliumGLIA, Issue 1 2001Monica M. Jablonski Abstract In conditions in which the retinal pigment epithelium (RPE) is dystrophic, carries a genetic mutation, or is removed physically, Müller cells undergo degenerative changes that contribute to the retinal pathology. We previously demonstrated that pigment epithelium-derived factor (PEDF), a glycoprotein secreted by the RPE cells with neuroprotective and differentiation properties, protects against photoreceptor degeneration induced by RPE removal. The purpose of the present study was to analyze the putative gliosupportive activity of PEDF on Müller cells of RPE-deprived retinas and assess whether protection of Müller cells was correlated with improved photoreceptor outer segment assembly. Eyes were dissected from Xenopus laevis tadpoles, and the RPE was removed before culturing in medium containing purified PEDF, PEDF plus anti-PEDF, or medium alone. Control eyes matured with an adherent RPE or in medium containing PEDF plus nonimmune serum. Müller cell ultrastructure was examined. Glial fibrillary acidic protein (GFAP) and glutamine synthetase were localized immunocytochemically, and the corresponding protein levels were quantified. In control retinas, Müller cells were structurally intact and formed adherens junctions with neighboring photoreceptors. In addition, they did not express GFAP, whereas glutamine synthetase expression was high. RPE removal dramatically altered the ultrastructure and biosynthetic activity of Müller cells; Müller cells failed to form adherens junctions with photoreceptors and glutamine synthetase expression was suppressed. PEDF prevented the degenerative glial response; Müller cells were ultrastructurally normal and formed junctional complexes with photoreceptors. PEDF also preserved the expression of glutamine synthetase at near-normal levels. The morphogenetic effects of PEDF were blocked by the anti-PEDF antibody. Our study documents the glioprotective effects of PEDF and suggests that maintenance of the proper Müller cell ultrastructure and expression of glutamine synthetase may be necessary to support the proper assembly of photoreceptor outer segments. GLIA 35:14,25, 2001. © 2001 Wiley-Liss, Inc. [source] The role of retinoic acid in the morphogenesis of the neural tubeJOURNAL OF ANATOMY, Issue 4 2003L. Wilson Abstract We have examined the role of the signalling molecule, retinoic acid, in the process of neurulation and the subsequent growth and differentiation of the central nervous system using quail embryos that have developed in the absence of retinoic acid. Such retinoic acid-free embryos undergo abnormal neural tube formation in terms of its shape and structure, but the embryos do not display spina bifida or exencephaly. The neural tubes have a wider floor plate, a thicker roof plate and a different dorsoventral shape. Phalloidin staining and electron microscopy revealed alterations in the actin filaments and the junctional complexes of the cell layer lining the lumen. Initially the neural tubes proliferated at the same rate as normal, but later the proliferation rate declined drastically and neuronal differentiation was highly deficient. There were very few motoneurons extending neurites into the periphery, and within the neural tube axon trajectories were chaotic. These results reveal several functions for retinoic acid in the morphogenesis and growth of the neural tube, many of which can be explained by defective notochord signalling, but they do not suggest that this molecule plays a role in neural tube closure. [source] Irsogladine maleate counters the interleukin-1,-induced suppression in gap-junctional intercellular communication but does not affect the interleukin-1,-induced zonula occludens protein-1 levels in human gingival epithelial cellsJOURNAL OF PERIODONTAL RESEARCH, Issue 1 2008T. Fujita Background and Objective:, Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin-8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin-1, is involved in periodontal disease. Little is known, however, about the effect of interleukin-1, on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin-1,. In this study, we examined how interleukin-1, affected gap junctional intercellular communication, connexin 43 and zonula occludens protein-1, and how irsogladine maleate modulated the interleukin-1,-induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods:, Human gingival epithelial cells were exposed to interleukin-1,, with or without irsogladine maleate. Connexin 43 and zonula occludens protein-1 were examined at mRNA and protein levels by real-time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of zonula occludens protein-1 was also confirmed by immunofluorescence. Results:, Interleukin-1, decreased connexin 43 mRNA levels, but increased zonula occludens protein-1 mRNA levels. Irsogladine maleate countered the interleukin-1,-induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased zonula occludens protein-1 levels. Conclusion:, The effect of interleukin-1, on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis. [source] Insulin aggregation and asymmetric transport across human bronchial epithelial cell monolayers (Calu-3)JOURNAL OF PHARMACEUTICAL SCIENCES, Issue 4 2002Isabelle Pezron Abstract The purpose of this work was to elucidate the transport pathways of zinc insulin across the Calu-3 cell monolayer, an in vitro model of the human airway epithelium. Calu-3 cells grown in liquid-covered conditions formed a confluent monolayer with a high transepithelial electrical resistance value of 1000,±,150 ,,·,cm2. The cell monolayer was characterized by a low mannitol permeability of 4.7,±,0.5 10,7cm/s. Transport of zinc insulin (donor concentration 1 U/mL) in Dulbecco's modified phosphate buffer saline at 37°C was found to be higher in the basolateral (BL) to apical (AP) (Papp,=,3.0,±,0.2 10,8 cm/s), than in the AP to BL direction (Papp,=,0.41,±,0.02 10,8 cm/s). P-glycoprotein efflux or specific enzymatic degradation did not appear to contribute toward this asymmetric transport. Insulin receptors, though apparently more abundant on the BL side than on the AP side of Calu-3 cells, did not mediate the direction-dependent transport of insulin. However, transport of a monomeric human insulin analog, Asp(B10)des(B28-30), across the Calu-3 cell monolayer was similar in both directions (BL to AP and AP to BL). The corresponding permeability, Papp,=,2.9,±,0.2 10,8 cm/s, was not significantly different from the permeability of zinc insulin in the BL to AP direction. The paracellular pathway seems to play a major role in the insulin transport across the Calu-3 cell monolayers. We hypothesize that the transport of zinc insulin oligomers is restricted at the AP surface by the presence of the tight junctional complexes. From the BL side, oligomers may undergo dissociation in the intercellular space and diffuse readily as monomers to the AP surface of the membrane. © 2002 Wiley-Liss, Inc. and the American Pharmaceutical Association J Pharm Sci 91:1135,1146, 2002 [source] Markers for the lymphatic endothelium: In search of the holy grail?MICROSCOPY RESEARCH AND TECHNIQUE, Issue 2 2001Jonathan P. Sleeman Abstract The ability to discriminate reliably at the histological level between blood and lymphatic microcapillaries would greatly assist the study of a number of biological and pathological questions and may also be of clinical utility. A structure,function comparison of these types of microcapillary suggests that differences which could function as markers to allow discrimination between blood and lymphatic endothelium should exist. Indeed, to date a variety of such markers have been proposed, including basement membrane components, constituents of junctional complexes such as desmoplakin and enzymes such as 5,-nucleotidase. Additionally, a variety of cell surface molecules are thought to be differentially expressed, including PAL-E, VEGFR-3, podoplanin, and LYVE-1. Several of the lymphatic markers proposed in the literature require further characterization to demonstrate fully their lymphatic specificity and some have proven not to be reliable. The relative merits and drawbacks of each of the proposed markers is discussed. Microsc. Res. Tech. 55:61,69, 2001. © 2001 Wiley-Liss, Inc. [source] Astroblastoma: Immunohistochemical and ultrastructural study of distinctive epithelial and probable tanycytic differentiationNEUROPATHOLOGY, Issue 1 2006Toshihiko Kubota We report the clinicopathological findings of astroblastoma found in an 8-year-old girl who was subsequently treated for 11 years. The primary superficially circumscribed tumor was located in the frontoparietal lobe, while the recurrent and the second recurrent tumor were restricted to the same region 11 years later. The tumors obtained on these three occasions showed fundamentally the same histological, immunohistochemical and fine structural features. They exhibited astrocytic as well as ependymal tanycytic features with apparent epithelial cell lineage. The tumor cells showed typical features of astroblastoma comprising prominent perivascular pseudorosettes with remarkable vascular sclerosis. The immunohistochemical study revealed intensive positivity of GFAP, vimentin, epithelial membrane antigen (EMA), cytokeratin, connexin 26 and 32, desmocollin 1 and neuronal cadherin. The fine structure revealed divergent types of junctional complexes, some of which were connected with tonofilament bundles. Numerous microvilli protruded and basal lamina abutted on the tumor cell surface. We report these unique histological features, and stress that astroblastoma should be categorized as a specific type of neuroepithelial tumor. [source] Astroglial structures in the zebrafish brain,THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 21 2010Larissa Grupp Abstract To understand components shaping the neuronal environment we studied the astroglial cells in the zebrafish brain using immunocytochemistry for structural and junctional markers, electron microscopy including freeze fracturing, and probed for the water channel protein aquaporin-4. Glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) showed largely overlapping immunoreactivity: GFAP in the main glial processes and GS in main processes and smaller branches. Claudin-3 immunoreactivity was spread in astroglial cells along their major processes. The ventricular lining was immunoreactive for the tight-junction associated protein ZO-1, in the telencephalon located on the dorsal, lateral, and medial surface due to the everting morphogenesis. In the tectum, subpial glial endfeet were also positive for ZO-1. Correspondingly, electron microscopy revealed junctional complexes between subpial glial endfeet. However, in freeze-fracture analysis tight junctional strands were not found between astroglial membranes, either in the optic tectum or in the telencephalon. Occurrence of aquaporin-4, the major astrocytic water channel in mammals, was demonstrated by polymerase chain reaction (PCR) analysis and immunocytochemistry in tectum and telencephalon. Localization of aquaporin-4 was not polarized but distributed along the entire radial extent of the cell. Interestingly, their membranes were devoid of the orthogonal arrays of particles formed by aquaporin-4 in mammals. Finally, we investigated astroglial cells in proliferative areas. Brain lipid basic protein, a marker of early glial differentiation but not GS, were present in some proliferation zones, whereas cells lining the ventricle were positive for both markers. Thus, astroglial cells in the zebrafish differ in many aspects from mammalian astrocytes. J. Comp. Neurol. 518:4277,4287, 2010. © 2010 Wiley-Liss, Inc. [source] Renal pathology of polycystic kidney disease and concurrent hereditary nephritis in Bull TerriersAUSTRALIAN VETERINARY JOURNAL, Issue 6 2002CA O'LEARY Objective To describe the renal lesions in Bull Terrier poly-cystic kidney disease (BTPKD), to confirm that the renal cysts in BTPKD arise from the nephron or collecting tubule, and to identify lesions consistent with concurrent BTPKD and Bull Terrier hereditary nephritis (BTHN). Design Renal tissue from five Bull Terriers with BTPKD and eight control dogs was examined by light and transmission electron microscopy. Clinical data were collected from all dogs, and family history of BTPKD and BTHN for all Bull Terriers. Results In BTPKD the renal cysts were lined by epithelial cells of nephron or collecting duct origin that were usually squamous or cuboidal, with few organelles. They had normal junctional complexes, and basal laminae of varying thicknesses. Glomeruli with small, atrophic tufts and dilated Bowman's capsules, tubular loss and dilation, and interstitial inflammation and fibrosis were common. Whereas the lesions seen in BTHN by light microscope were nonspecific, the presence of characteristic ultrastructural glomerular basement membrane (GMB) lesions and a family history of this disease indicated concurrent BTHN was likely in three of five cases of BTPKD. Conclusion This paper provides evidence that renal cysts in BTPKD are of nephron or collecting duct origin. In addition, GBM lesions are described that strongly suggest that BTPKD and BTHN may occur simultaneously. 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