Morphological changes in gallbladder epithelial cells in histological, scraped cytological, and bile specimens-A morphometric study based on nuclear and cytoplasmic point counting-

Dispersal of epithelial cells is an important aspect of tumorigenesis, and invasion. Factors such as hepatocyte growth factor induce the breakdown of cell junctions and promote cell spreading and the dispersal of colonies of epithelial cells, providing a model system to investigate the biochemical signals that regulate these events. Multiple signaling proteins are phosphorylated in epithelial cells during hepatocyte growth factor–induced cell dispersal, including c-Cbl, a protooncogene docking protein with ubiquitin ligase activity. We have examined the role of c-Cbl and a transforming variant (70z-Cbl) in epithelial cell dispersal. We show that the expression of 70z-Cbl in Madin-Darby canine kidney epithelial cells resulted in the breakdown of cell–cell contacts and alterations in cell morphology characteristic of epithelial–mesenchymal transition. Structure–function studies revealed that the amino-terminal portion of c-Cbl, which corresponds to the Cbl phosphotyrosine-binding/Src homology domain 2 , is sufficient to promote the morphological changes in cell shape. Moreover, a point mutation at Gly-306 abrogates the ability of the Cbl Src homology domain 2 to induce these morphological changes. Our results identify a role for Cbl in the regulation of epithelial–mesenchymal transition, including loss of adherens junctions, cell spreading, and the initiation of cell dispersal.

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Vibrio choleraehemagglutinin/protease (HA/protease) causes morphological changes in cultured epithelial cells and perturbs their paracellular barrier function

Microbial Pathogenesis ◽

10.1006/mpat.1996.0047 ◽

1996 ◽

Vol 21 (2) ◽

pp. 111-123 ◽

Cited By ~ 57

Author(s):

Zhengyang Wu ◽

Debra Milton ◽

Pia Nybom ◽

Anita Sjö ◽

Karl-Eric Magnusson

Keyword(s):

Epithelial Cells ◽

Barrier Function ◽

Morphological Changes ◽

Cultured Epithelial Cells

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An asymmetric junctional mechanoresponse coordinates mitotic rounding with epithelial integrity

The Journal of Cell Biology ◽

10.1083/jcb.202001042 ◽

2021 ◽

Vol 220 (5) ◽

Author(s):

Jooske L. Monster ◽

Lisa Donker ◽

Marjolein J. Vliem ◽

Zaw Win ◽

Helen K. Matthews ◽

...

Keyword(s):

Epithelial Cells ◽

Morphological Changes ◽

Mitotic Cell ◽

Cell Junctions ◽

Actin Binding ◽

Epithelial Barrier ◽

Epithelial Integrity ◽

Tensile Forces ◽

Shape Changes ◽

Mitotic Cells

Epithelia are continuously self-renewed, but how epithelial integrity is maintained during the morphological changes that cells undergo in mitosis is not well understood. Here, we show that as epithelial cells round up when they enter mitosis, they exert tensile forces on neighboring cells. We find that mitotic cell–cell junctions withstand these tensile forces through the mechanosensitive recruitment of the actin-binding protein vinculin to cadherin-based adhesions. Surprisingly, vinculin that is recruited to mitotic junctions originates selectively from the neighbors of mitotic cells, resulting in an asymmetric composition of cadherin junctions. Inhibition of junctional vinculin recruitment in neighbors of mitotic cells results in junctional breakage and weakened epithelial barrier. Conversely, the absence of vinculin from the cadherin complex in mitotic cells is necessary to successfully undergo mitotic rounding. Our data thus identify an asymmetric mechanoresponse at cadherin adhesions during mitosis, which is essential to maintain epithelial integrity while at the same time enable the shape changes of mitotic cells.

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Morphometric study of the platform elements of Amydrotaxis praejohnsoni n. sp. (Lower Devonian, conodonts, Nevada)

Journal of Paleontology ◽

10.1017/s002233600001951x ◽

1989 ◽

Vol 63 (3) ◽

pp. 349-355 ◽

Cited By ~ 6

Author(s):

Michael A. Murphy ◽

Kathleen B. Springer

Keyword(s):

Lower Devonian ◽

Morphological Changes ◽

Morphometric Study ◽

Mosaic Pattern ◽

Basal Cavity

The platform element of the conodont Amydrotaxis praejohnsoni n. sp. shows statistically significant morphological changes from the base to the top of the delta Zone (Lower Devonian). The changes occur particularly in mean denticle number, height and character of the anterior denticles, and shape of the basal cavity. The earliest forms have fewer denticles ( = 7.1), an enlarged, high anterior denticle, and a broadly flared posterior basal cavity, whereas late forms have more denticles ( = 9.4), equal-sized anterior denticles, and a narrow posterior basal cavity. There is no stasis phase in the species history, but rather a mosaic pattern in which the observed changes in the character states are seemingly independent of each other and proceed at variable rates.

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Lactobacillus fermentum UCO-979C beneficially modulates the innate immune response triggered by Helicobacter pylori infection in vitro

Beneficial Microbes ◽

10.3920/bm2018.0019 ◽

2018 ◽

Vol 9 (5) ◽

pp. 829-841 ◽

Cited By ~ 7

Author(s):

V. Garcia-Castillo ◽

H. Zelaya ◽

A. Ilabaca ◽

M. Espinoza-Monje ◽

R. Komatsu ◽

...

Keyword(s):

Immune Response ◽

Helicobacter Pylori ◽

Epithelial Cells ◽

Morphological Changes ◽

Helicobacter Pylori Infection ◽

Lactobacillus Fermentum ◽

Gastric Tissue ◽

Gastric Epithelial Cells ◽

Ags Cells ◽

H Pylori

Helicobacter pylori infection is associated with important gastric pathologies. An aggressive proinflammatory immune response is generated in the gastric tissue infected with H. pylori, resulting in gastritis and a series of morphological changes that increase the susceptibility to cancer development. Probiotics could present an alternative solution to prevent or decrease H. pylori infection. Among them, the use of immunomodulatory lactic acid bacteria represents a promising option to reduce the severity of chronic inflammatory-mediated tissue damage and to improve protective immunity against H. pylori. We previously isolated Lactobacillus fermentum UCO-979C from human gastric tissue and demonstrated its capacity to reduce adhesion of H. pylori to human gastric epithelial cells (AGS cells). In this work, the ability of L. fermentum UCO-979C to modulate immune response in AGS cells and PMA phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 (human monocytic leukaemia) macrophages in response to H. pylori infection was evaluated. We demonstrated that the UCO-979C strain is able to differentially modulate the cytokine response of gastric epithelial cells and macrophages after H. pylori infection. Of note, L. fermentum UCO-979C was able to significantly reduce the production of inflammatory cytokines and chemokines in AGS and THP-1 cells as well as increase the levels of immunoregulatory cytokines, indicating a remarkable anti-inflammatory effect. These findings strongly support the probiotic potential of L. fermentum UCO-979C and provide evidence of its beneficial effects against the inflammatory damage induced by H. pylori infection. Although our findings should be proven in appropriate experiments in vivo, in both H. pylori infection animal models and human trials, the results of the present work provide a scientific rationale for the use of L. fermentum UCO-979C to prevent or reduce H. pylori-induced gastric inflammation in humans.

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Features of morphological changes in the intramural nervous system of the heart in atherosclerosis and myocardial infarction

Kazan medical journal ◽

10.17816/kazmj64151 ◽

1980 ◽

Vol 61 (4) ◽

pp. 26-28

Author(s):

M. V. Uglova ◽

V. N. Shlyapnikov ◽

V. V. Sergeev ◽

A. U. Zalmunin ◽

E. A. Taikov

Keyword(s):

Myocardial Infarction ◽

Nervous System ◽

Morphological Changes ◽

Morphometric Study ◽

Hypertrophic Changes

Morphometric study of human cardiac neurocytes in myocardial infarction and atherosclerosis made it possible to establish that myocardial infarction causes adaptive (hypertrophic) changes in the intramural nervous system of the heart, especially pronounced on the first day of the course of the infarction; with atherosclerosis, the changes are characterized by a direction towards atrophic processes.

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Monochloramine induces reorganization of nuclear speckles and phosphorylation of SRp30 in human colonic epithelial cells: role of protein kinase C

AJP Cell Physiology ◽

10.1152/ajpcell.00090.2003 ◽

2003 ◽

Vol 285 (5) ◽

pp. C1294-C1303 ◽

Cited By ~ 8

Author(s):

Ya-Qin Zhu ◽

Yu Lu ◽

Xiao-Di Tan

Keyword(s):

Gastrointestinal Tract ◽

Epithelial Cells ◽

Intestinal Epithelial Cells ◽

Morphological Changes ◽

Sr Proteins ◽

Mrna Splicing ◽

Intestinal Epithelial ◽

Nuclear Speckles ◽

Colonic Epithelial Cells ◽

Stimulation Of

Intestinal epithelial cells are constantly stimulated by reactive oxidant metabolites (ROMs) in inflamed mucosa. Monochloramine (NH2Cl), a cell-permeant ROM, is particularly relevant to the pathogenesis of inflammation in the gastrointestinal tract. Nuclear speckles, a unique nuclear subcompartment, accumulate a family of proteins, namely, serine- and arginine-rich (SR) proteins. They play important roles in regulation of pre-mRNA splicing. Currently, little is known about the link between inflammatory stimulation and the pre-mRNA splicing process, although gene expression is changed in inflamed tissues. The present study was designed to investigate whether stimulation of human colonic epithelial cells (HT-29 and Caco-2 cell lines) with NH2Cl affects nuclear speckles and their components. By indirect immunofluorescence, nuclear speckles have been shown to undergo rapid aggregation after NH2Cl stimulation. By utilizing Western blotting, SRp30 (a subset of SR proteins) in intestinal epithelial cells was found to be phosphorylated after NH2Cl treatment, whereas other SR proteins were not responsive to NH2Cl stimulation. The cytotoxic effect of NH2Cl was excluded by both negative lactate dehydrogenase assay and propidium iodide staining. Therefore, NH2Cl-induced morphological changes on nuclear speckles and phosphorylated SRp30 do not result from intestinal epithelial injury. Furthermore, the effect of NH2Cl on nuclear speckles and SRp30 was blocked by bisindolylmaleimide I, a selective PKC inhibitor. Together, the available data suggest that stimulation of intestinal epithelial cells with NH2Cl results in a consequent change on pre-mRNA splicing machinery via a distinctive signal pathway involving activation of PKC. This effect may contribute to oxidant-induced pathophysiological changes in the gastrointestinal tract.

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