scholarly journals Transcriptional and Ultrastructural Analyses Suggest Novel Insights into Epithelial Barrier Impairment in Celiac Disease

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 516
Author(s):  
Agnieszka Sowińska ◽  
Yasser Morsy ◽  
Elżbieta Czarnowska ◽  
Beata Oralewska ◽  
Ewa Konopka ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Epithelial Cells ◽  
Intestinal Permeability ◽  
Transcriptional Analysis ◽  
Junctional Complex ◽  
Sequencing Data ◽  
Ultrastructural Studies ◽  
Extracellular Region ◽  
Significant Gene

Disruption of epithelial junctional complex (EJC), especially tight junctions (TJ), resulting in increased intestinal permeability, is supposed to activate the enhanced immune response to gluten and to induce the development of celiac disease (CD). This study is aimed to present the role of EJC in CD pathogenesis. To analyze differentially expressed genes the next-generation mRNA sequencing data from CD326+ epithelial cells isolated from non-celiac and celiac patients were involved. Ultrastructural studies with morphometry of EJC were done in potential CD, newly recognized active CD, and non-celiac controls. The transcriptional analysis suggested disturbances of epithelium and the most significant gene ontology enriched terms in epithelial cells from CD patients related to the plasma membrane, extracellular exome, extracellular region, and extracellular space. Ultrastructural analyses showed significantly tighter TJ, anomalies in desmosomes, dilatations of intercellular space, and shorter microvilli in potential and active CD compared to controls. Enterocytes of fetal-like type and significantly wider adherence junctions were observed only in active CD. In conclusion, the results do not support the hypothesis that an increased passage of gluten peptides by unsealing TJ precedes CD development. However, increased intestinal permeability due to abnormality of epithelium might play a role in CD onset.

scholarly journals Immunopathology of childhood celiac disease—Key role of intestinal epithelial cells

PLoS ONE ◽  
2017 ◽  
Vol 12 (9) ◽  
pp. e0185025 ◽  
Author(s):  
Grzegorz Pietz ◽  
Rituparna De ◽  
Maria Hedberg ◽  
Veronika Sjöberg ◽  
Olof Sandström ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals Rho/Rho-associated Kinase-II Signaling Mediates Disassembly of Epithelial Apical Junctions

2007 ◽  
Vol 18 (9) ◽  
pp. 3429-3439 ◽  
Author(s):  
Stanislav N. Samarin ◽  
Andrei I. Ivanov ◽  
Gilles Flatau ◽  
Charles A. Parkos ◽  
Asma Nusrat
Keyword(s):  
Epithelial Cells ◽  
Rho Gtpase ◽  
Critical Role ◽  
Junctional Complex ◽  
Nucleotide Exchange ◽  
Calcium Depletion ◽  
Pharmacological Inhibition ◽  
Apical Junctional Complex ◽  
Apical Junctions

Apical junctional complex (AJC) plays a vital role in regulation of epithelial barrier function. Disassembly of the AJC is observed in diverse physiological and pathological states; however, mechanisms governing this process are not well understood. We previously reported that the AJC disassembly is driven by the formation of apical contractile acto-myosin rings. In the present study, we analyzed the signaling pathways regulating acto-myosin–dependent disruption of AJC by using a model of extracellular calcium depletion. Pharmacological inhibition analysis revealed a critical role of Rho-associated kinase (ROCK) in AJC disassembly in calcium-depleted epithelial cells. Furthermore, small interfering RNA (siRNA)-mediated knockdown of ROCK-II, but not ROCK-I, attenuated the disruption of the AJC. Interestingly, AJC disassembly was not dependent on myosin light chain kinase and myosin phosphatase. Calcium depletion resulted in activation of Rho GTPase and transient colocalization of Rho with internalized AJC proteins. Pharmacological inhibition of Rho prevented AJC disassembly. Additionally, Rho guanine nucleotide exchange factor (GEF)-H1 translocated to contractile F-actin rings after calcium depletion, and siRNA-mediated depletion of GEF-H1 inhibited AJC disassembly. Thus, our findings demonstrate a central role of the GEF-H1/Rho/ROCK-II signaling pathway in the disassembly of AJC in epithelial cells.

scholarly journals Regulation of desmosome assembly in MDCK epithelial cells: coordination of membrane core and cytoplasmic plaque domain assembly at the plasma membrane.

1991 ◽  
Vol 113 (3) ◽  
pp. 645-655 ◽  
Author(s):  
M Pasdar ◽  
K A Krzeminski ◽  
W J Nelson
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Sucrose Gradient ◽  
Integral Membrane Proteins ◽  
Junctional Complex ◽  
Immunofluorescence Analysis ◽  
Cell Biol ◽  
Cytoskeletal Elements ◽  
Triton X

Desmosomes are major components of the intercellular junctional complex in epithelia. They consist of at least eight different cytoplasmic and integral membrane proteins that are organized into two biochemically and structurally distinct domains: the cytoplasmic plaque and membrane core. We showed previously that in MDCK epithelial cells major components of the cytoplasmic plaque (desmoplakin I and II; DPI/II) and membrane core domains (desmoglein I; DGI) initially enter a pool of proteins that is soluble in buffers containing Triton X-100, and then titrate into an insoluble pool before their arrival at the plasma membrane (Pasdar, M., and W. J. Nelson. 1988. J. Cell Biol. 106:677-685; Pasdar. M., and W. J. Nelson. 1989. J. Cell Biol. 109:163-177). We have now examined whether either the soluble or insoluble pool of these proteins represents an intracellular site for assembly and interactions between the domains before their assembly into desmosomes at the plasma membrane. Interactions between the Triton X-100-soluble pools of DPI/II and DGI were analyzed by sedimentation of extracted proteins in sucrose gradients. Results show distinct differences in the sedimentation profiles of these proteins, suggesting that they are not associated in the Triton X-100-soluble pool of proteins; this was also supported by the observation that DGI and DPI/II could not be coimmunoprecipitated in a complex with each other from sucrose gradient fractions. Immunofluorescence analysis of the insoluble pools of DPI/II and DGI, in cells in which desmosome assembly had been synchronized, showed distinct differences in the spatial distributions of these proteins. Furthermore, DPI/II and DGI were found to be associated with different elements of cytoskeleton; DPI/II were located along cytokeratin intermediate filaments, whereas DGI appeared to be associated with microtubules. The regulatory role of cytoskeletal elements in the intracellular organization and assembly of the cytoplasmic plaque and membrane core domains, and their integration into desmosomes on the plasma membrane is discussed.

Effect of Calcium on the Growth and Differentiation of Cultured Rat Esophageal Epithelial Cells

1982 ◽  
Vol 40 ◽  
pp. 132-133
Author(s):  
W.T. Gunning ◽  
M.R. Marino ◽  
M.S. Babcock ◽  
G.D. Stoner
Keyword(s):  
Epithelial Cells ◽  
Cell Types ◽  
Replication Rate ◽  
Enzymatic Dissociation ◽  
Growth Assay ◽  
Epidermal Growth ◽  
Fetal Bovine ◽  
Esophageal Epithelial Cells ◽  
Cellular Replication

The role of calcium in modulating cellular replication and differentiation has been described for various cell types. In the present study, the effects of Ca++ on the growth and differentiation of cultured rat esophageal epithelial cells was investigated.Epithelial cells were isolated from esophagi taken from 8 week-old male CDF rats by the enzymatic dissociation method of Kaighn. The cells were cultured in PFMR-4 medium supplemented with 0.25 mg/ml dialyzed fetal bovine serum, 5 ng/ml epidermal growth factor, 10-6 M hydrocortisone 10-6 M phosphoethanolamine, 10-6 M ethanolamine, 5 pg/ml insulin, 5 ng/ml transferrin, 10 ng/ml cholera toxin and 50 ng/ml garamycin at 36.5°C in a humidified atmosphere of 3% CO2 in air. At weekly intervals, the cells were subcultured with a solution containing 1% polyvinylpyrrolidone, 0.01% EGTA, and 0.05% trypsin. After various passages, the replication rate of the cells in PFMR-4 medium containing from 10-6 M to 10-3 M Ca++ was determined using a clonal growth assay.

Adenomatoid Tumor of the Testis, A Mesonephric Hamartoma

1971 ◽  
Vol 29 ◽  
pp. 318-319
Author(s):  
Raoul Fresco ◽  
Mary Chang-Lo
Keyword(s):  
Electron Microscopy ◽  
Epithelial Cells ◽  
Fibrous Tissue ◽  
Salient Feature ◽  
Luminal Surface ◽  
Adenomatoid Tumor ◽  
Ultrastructural Studies ◽  
Epithelial Origin ◽  
Brush Borders ◽  
Cell Processes

Confusion surrounds the nature of the “adenomatoid tumor” of the testis, as evidenced by the large number of synonyms which have been ascribed to it. Various authors have considered the tumor to be of endothelial, mesothelial or epithelial origin. There appears to be no controversy as to the stromal elements of the tumor, which consists mainly of smooth muscle and fibrous tissue. It is the irregular gland-like spaces which have given rise to the numerous theories as to its histogenesis, and even recent ultrastructural studies fail to agree on the origin of these structures.Electron microscopy of a typical intrascrotal adenomatoid tumor showed the gland-like spaces to be lined by epithelial cells (Fig. 1), rich in cytoplasmic tonofibrils and united to each other by numerous desmosomes (Fig. 2). The most salient feature of these epithelial cells was the presence on their luminal surface of numerous long and repeatedly branching microvillous structures of the type known as stereocilia (Fig. 3). These are extremely long slender cell processes which are as much as three to four times the length of those in brush borders.

Role of Bronchial Epithelial Cells in Pathogenesis of COPD

Pneumologie ◽  
2011 ◽  
Vol 65 (12) ◽  
Author(s):  
S Rim ◽  
S Jahan ◽  
G John ◽  
K Kohse ◽  
A Bohla ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial

ROLE OF THE NOVEL INTRODUCED PAN-INTESTINAL CAPSULE ENDOSCOPY SYSTEM IN CELIAC DISEASE

2019 ◽  
Author(s):  
F Foerster ◽  
K Mönkemüller ◽  
PR Galle ◽  
H Neumann
Keyword(s):  
Celiac Disease ◽  
Capsule Endoscopy ◽  
The Novel
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