Hydra regeneration from recombined ectodermal and endodermal tissue. I. Epibolic ectodermal spreading is driven by cell intercalation

1996 ◽  
Vol 109 (4) ◽  
pp. 763-772 ◽  
Author(s):  
Y. Kishimoto ◽  
M. Murate ◽  
T. Sugiyama
Keyword(s):  
Contact Surface ◽  
Single Cells ◽  
Cell Interaction ◽  
Inhibitory Effect ◽  
Cell Aggregates ◽  
Signaling Mechanism ◽  
Initial Adhesion ◽  
Radial Cell ◽  
Epithelial Sheet ◽  
Cell Intercalation

Cell-cell interaction and cell rearrangement were examined in the process of epithelial sheet formation during regeneration from hydra cell aggregates. The ectodermal and endodermal epithelial cell layers of Hydra magnipapillata were separated by procaine treatment. Each of the separated layers was then dissociated into single cells and reaggregated to produce ectodermal or endodermal cell aggregates. When the two aggregate types were recombined, a firm adhesion was quickly established between them. This was followed by a vigorous spreading of the ectodermal epithelial cells as a thin layer over the endoderm in a manner similar to the ‘epiboly’ in some developing embryos. Cell movement in this spreading process was examined using fluorescent dyestaining. It revealed that cells initially located in the inside of the aggregate migrated to intercalate themselves among the cells originally present in the contact surface. This radial cell intercalation took place continuously in the contact surface of both the ectodermal and endodermal aggregates, and produced a rapid growth of the contact surface, eventually leading to complete envelopment of the entire endoderm by the ectoderm. The resulting structure was a small sphere having a two-layered epithelial organization as in normal hydra. This sphere regenerated into a complete hydra a few days later. A tryptic extract of hydra membrane fraction specifically inhibited the ectodermal spreading over the endoderm, but not the initial adhesion or the later regeneration processes. These observations suggest that radial cell intercalation at the contact surface plays a crucial role in producing ectodermal spreading and establishing epithelial sheet organization in the recombined aggregates. The intercalation is presumably activated by a signal exchange through the contact surface. The inhibitory effect of the membrane extract suggests that it contains a factor that is involved in some way in this signaling mechanism.

Effects of carbamylcholine on chick embryo aggregate retina cell cultures

1988 ◽  
Vol 46 ◽  
pp. 350-351
Author(s):  
Glenn M. Cohen ◽  
Radharaman Ray
Keyword(s):  
Cell Cultures ◽  
Single Cells ◽  
Retinal Cell ◽  
Cell Aggregates ◽  
High Concentration ◽  
In Ovo ◽  
Sterile Culture ◽  
Retinal Tissue ◽  
Synaptic Junctions ◽  
And Control

Retinal,cell aggregates develop in culture in a pattern similar to the in ovo retina, forming neurites first and then synapses. In the present study, we continuously exposed chick retinal cell aggregates to a high concentration (1 mM) of carbamylcholine (carbachol), an acetylcholine (ACh) analog that resists hydrolysis by acetylcholinesterase (AChE). This situation is similar to organophosphorus anticholinesterase poisoning in which the ACh level is elevated at synaptic junctions due to inhibition of AChE, Our objective was to determine whether continuous carbachol exposure either damaged cholino- ceptive neurites, cell bodies, and synaptic elements of the aggregates or influenced (hastened or retarded) their development.The retinal tissue was isolated aseptically from 11 day embryonic White Leghorn chicks and then enzymatically (trypsin) and mechanically (trituration) dissociated into single cells. After washing the cells by repeated suspension and low (about 200 x G) centrifugation twice, aggregate cell cultures (about l0 cells/culture) were initiated in 1.5 ml medium (BME, GIBCO) in 35 mm sterile culture dishes and maintained as experimental (containing 10-3 M carbachol) and control specimens.

scholarly journals Unipolar distributions of junctional Myosin II identify cell stripe boundaries that drive cell intercalation throughout Drosophila axis extension

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Robert J Tetley ◽  
Guy B Blanchard ◽  
Alexander G Fletcher ◽  
Richard J Adams ◽  
Bénédicte Sanson
Keyword(s):  
Myosin Ii ◽  
Interaction Model ◽  
Cell Interaction ◽  
Cell Number ◽  
Cell Polarization ◽  
Convergence And Extension ◽  
Pair Rule Gene ◽  
Cell Intercalation ◽  
Pair Rule ◽  
Cell Cell

Convergence and extension movements elongate tissues during development. Drosophila germ-band extension (GBE) is one example, which requires active cell rearrangements driven by Myosin II planar polarisation. Here, we develop novel computational methods to analyse the spatiotemporal dynamics of Myosin II during GBE, at the scale of the tissue. We show that initial Myosin II bipolar cell polarization gives way to unipolar enrichment at parasegmental boundaries and two further boundaries within each parasegment, concomitant with a doubling of cell number as the tissue elongates. These boundaries are the primary sites of cell intercalation, behaving as mechanical barriers and providing a mechanism for how cells remain ordered during GBE. Enrichment at parasegment boundaries during GBE is independent of Wingless signaling, suggesting pair-rule gene control. Our results are consistent with recent work showing that a combinatorial code of Toll-like receptors downstream of pair-rule genes contributes to Myosin II polarization via local cell-cell interactions. We propose an updated cell-cell interaction model for Myosin II polarization that we tested in a vertex-based simulation.

The effects of tumour cells on embryonic cell aggregation, adhesion and detachment

1978 ◽  
Vol 29 (1) ◽  
pp. 271-275
Author(s):  
D.E. Maslow ◽  
L. Weiss
Keyword(s):  
Aggregate Size ◽  
Cell Aggregation ◽  
Inhibitory Effect ◽  
Neural Retina ◽  
Embryonic Cell ◽  
Tumour Cells ◽  
Ehrlich Ascites ◽  
Initial Adhesion ◽  
Ehrlich Ascites Cells ◽  
Gyratory Shaker

The presence of small numbers of tumour cells inhibits the aggregation of embryonic chicken neural retina cells grown in gyratory shaker culture. The aggregation of neural retina cells was also inhibited by ascites cell medium. We investigated whether the inhibitory effect of the tumour cells on aggregate size is effected by inhibition of the initial adhesion or by enhancement of their separation. The number of neural retina cells adherent to microtest plate surfaces was significantly reduced after incubation with either Ehrlich ascites cells or cell-free, conditioned medium, while the percentage of cells removed from glass by shearing was unchanged under those conditions. These results suggest that the reduction in neural retina cell aggregate size produced by Ehrlich ascites cells and their products is due to partial inhibition of neural retina cell adhesion processes, as distinct from enhancement of separation.

scholarly journals Inhibitory Effect of Centella asiatica Extract on DNCB-Induced Atopic Dermatitis in HaCaT Cells and BALB/c Mice

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 411 ◽  
Author(s):  
Yonghyeon Lee ◽  
Hyeon Kyeong Choi ◽  
Kaudjhis Patrick Ulrich N’deh ◽  
Young-Jin Choi ◽  
Meiqi Fan ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Allergic Inflammation ◽  
Centella Asiatica ◽  
Ethanol Extract ◽  
Inhibitory Effect ◽  
Interferon Γ ◽  
Dependent Manner ◽  
Hacat Cells ◽  
Signaling Mechanism ◽  
Tnf Α

Atopic dermatitis (AD) is a chronic inflammatory skin disease caused mainly by immune dysregulation. This study explored the anti-inflammatory and immunomodulatory effects of the Centella asiatica ethanol extract (CA) on an AD-like dermal disorder. Treatment with CA inhibited the expression of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in a dose-dependent manner in inflammatory stimulated HaCaT cells by interferon-γ (IFN-γ) and TNF-α-triggered inflammation. Eight-week-old BALB/c mice treated with 2,4-dinitrochlorobenzene (DNCB) were used as a mouse model of AD. In AD induce model, we had two types treatment of CA; skin local administration (80 µg/cm2, AD+CA-80) and oral administration (200 mg/kg/d, AD+CA-200). Interestingly, the CA-treated groups exhibited considerably decreased mast cell infiltration in the ear tissue. In addition, the expression of IL-6 in mast cells, as well as the expression of various pathogenic cytokines, such as TNF-α, IL-4, IL-5, IL-6, IL-10, IL-17, iNOS, COX-2, and CXCL9, was reduced in both AD+CA-80 and AD+CA-200 groups. Collectively, our data demonstrate the pharmacological role and signaling mechanism of CA in the regulation of allergic inflammation of the skin, which supports our hypothesis that CA could potentially be developed as a therapeutic agent for AD.

scholarly journals Regulation of transferrin-induced endocytosis by wild-type and C282Y-mutant HFE in transfected HeLa cells

2002 ◽  
Vol 282 (5) ◽  
pp. C973-C979 ◽  
Author(s):  
Lukas Schwake ◽  
Andreas W. Henkel ◽  
Hans D. Riedel ◽  
Thorsten Schlenker ◽  
Matthias Both ◽  
...  
Keyword(s):  
Hela Cells ◽  
Single Cells ◽  
Hereditary Hemochromatosis ◽  
Inhibitory Effect ◽  
Membrane Capacitance ◽  
Wild Type ◽  
Time Resolved ◽  
Cell Membrane Capacitance ◽  
Endocytic Vesicles ◽  
In Cells

The hereditary hemochromatosis protein HFE is known to complex with the transferrin receptor; however, its function regarding endocytosis of transferrin is unclear. We performed patch-clamp capacitance measurements in transfected HeLa cells carrying wild-type or C282Y-mutant HFE cDNA under the control of a tetracycline-sensitive promoter. Whole cell experiments in cells with suppressed expression of wild-type HFE revealed a decrease in membrane capacitance, reflecting predominance of endocytosis in the presence of transferrin. Cells overexpressing C282Y-mutant HFE displayed less intense capacitance decreases, whereas no significant decrease was observed in cells overexpressing wild-type HFE. The formation of single endocytic vesicles in cells with suppressed expression of wild-type HFE was greatly increased in the presence of transferrin as revealed by cell-attached recordings. According to their calculated diameters, many of these vesicles corresponded to clathrin-coated vesicles. These results suggest that wild-type HFE negatively modulates the endocytic uptake of transferrin. This inhibitory effect is attenuated in cells expressing C282Y-mutant HFE. Time-resolved measurements of cell membrane capacitance provide a powerful tool to study transferrin-induced endocytosis in single cells.

Micro-Raman spectroscopy in medicine

2019 ◽  
Vol 4 (10) ◽  
Author(s):  
Christoph Krafft ◽  
Jürgen Popp
Keyword(s):  
Raman Spectroscopy ◽  
Tissue Characterization ◽  
Point Of Care ◽  
Cell Metabolism ◽  
Single Cells ◽  
Cell Interaction ◽  
Diagnostic Tools ◽  
Clinical Tool ◽  
Micro Raman Spectroscopy ◽  
Molecular Specificity

Abstract A potential role of optical technologies in medicine including micro-Raman spectroscopy is diagnosis of bacteria, cells and tissues which is covered in this chapter. The main advantage of Raman-based methods to complement and augment diagnostic tools is that unsurpassed molecular specificity is achieved without labels and in a nondestructive way. Principles and applications of micro-Raman spectroscopy in the context of medicine will be described. First, Raman spectra of biomolecules representing proteins, nucleic acids, lipids and carbohydrates are introduced. Second, microbial applications are summarized with the focus on typing on species and strain level, detection of infections, antibiotic resistance and biofilms. Third, cytological applications are presented to classify single cells and study cell metabolism and drug–cell interaction. Fourth, applications to tissue characterization start with discussion of lateral resolution for Raman imaging followed by Raman-based detection of pathologies and combination with other modalities. Finally, an outlook is given to translate micro-Raman spectroscopy as a clinical tool to solve unmet needs in point-of-care applications and personalized treatment of diseases.

scholarly journals Role of F1C Fimbriae, Flagella, and Secreted Bacterial Components in the Inhibitory Effect of Probiotic Escherichia coli Nissle 1917 on Atypical Enteropathogenic E. coli Infection

2014 ◽  
Vol 82 (5) ◽  
pp. 1801-1812 ◽  
Author(s):  
Sylvia Kleta ◽  
Marcel Nordhoff ◽  
Karsten Tedin ◽  
Lothar H. Wieler ◽  
Rafal Kolenda ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Molecular Mechanisms ◽  
Inhibitory Effect ◽  
Host Cells ◽  
Single Infection ◽  
Content Type ◽  
E Coli ◽  
Initial Adhesion

ABSTRACTEnteropathogenicEscherichia coli(EPEC) is recognized as an important intestinal pathogen that frequently causes acute and persistent diarrhea in humans and animals. The use of probiotic bacteria to prevent diarrhea is gaining increasing interest. The probioticE. colistrain Nissle 1917 (EcN) is known to be effective in the treatment of several gastrointestinal disorders. While bothin vitroandin vivostudies have described strong inhibitory effects of EcN on enteropathogenic bacteria, including pathogenicE. coli, the underlying molecular mechanisms remain largely unknown. In this study, we examined the inhibitory effect of EcN on infections of porcine intestinal epithelial cells with atypical enteropathogenicE. coli(aEPEC) with respect to single infection steps, including adhesion, microcolony formation, and the attaching and effacing phenotype. We show that EcN drastically reduced the infection efficiencies of aEPEC by inhibiting bacterial adhesion and growth of microcolonies, but not the attaching and effacing of adherent bacteria. The inhibitory effect correlated with EcN adhesion capacities and was predominantly mediated by F1C fimbriae, but also by H1 flagella, which served as bridges between EcN cells. Furthermore, EcN seemed to interfere with the initial adhesion of aEPEC to host cells by secretion of inhibitory components. These components do not appear to be specific to EcN, but we propose that the strong adhesion capacities enable EcN to secrete sufficient local concentrations of the inhibitory factors. The results of this study are consistent with a mode of action whereby EcN inhibits secretion of virulence-associated proteins of EPEC, but not their expression.

Innovative Tools and Technology for Analysis of Single Cells and Cell–Cell Interaction

2016 ◽  
Vol 18 (1) ◽  
pp. 259-284 ◽  
Author(s):  
Tania Konry ◽  
Saheli Sarkar ◽  
Pooja Sabhachandani ◽  
Noa Cohen
Keyword(s):  
Single Cells ◽  
Cell Interaction ◽  
Cell Cell
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