scholarly journals A STUDY ON THE MECHANISM OF INTERCELLULAR ADHESION

1974 ◽  
Vol 60 (3) ◽  
pp. 641-652 ◽  
Author(s):  
Joris J. Deman ◽  
Erik A. Bruyneel ◽  
Marc M. Mareel
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Calcium Ions ◽  
Hela Cells ◽  
Previous Treatment ◽  
Cell Aggregation ◽  
Sialic Acids ◽  
Magnesium Ions ◽  
Trypsin Treatment ◽  
Calcium Effect

Aggregation of suspended HeLa cells is increased on removal of cell surface sialic acid. Calcium ions promote aggregation whereas magnesium ions have no effect. The calcium effect is abolished by previous treatment of the cells with neuraminidase. Trypsinization of the HeLa cells followed by thorough washing diminishes the rate of mutual cell aggregation. Subsequent incubation with neuraminidase restores the aggregation rate to the original value before trypsin treatment. Cells which had acquired a greater tendency for aggregation after removal of peripheral sialic acid lose this property when subsequently treated with trypsin. Calcium ions have no aggregative effect on trypsinized cells. In contrast to HeLa cells, aggregation of human erythrocytes was not increased after treatment with neuraminidase or on addition of calcium. The results with HeLa cells are interpreted as follows: (a) Trypsin-releasable material confers adhesiveness upon the cells. (b) The adhesive property of this material is counteracted by the presence of cell surface sialic acids. (c) Calcium ions exert their effect by attenuating the adverse effect of sialic acid.

Boronic acid recognition based-gold nanoparticle-labeling strategy for the assay of sialic acid expression on cancer cell surface by inductively coupled plasma mass spectrometry

The Analyst ◽  
2016 ◽  
Vol 141 (4) ◽  
pp. 1286-1293 ◽  
Author(s):  
Xing Zhang ◽  
Beibei Chen ◽  
Man He ◽  
Yuan Zhang ◽  
Lu Peng ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Sialic Acid ◽  
Cell Surface ◽  
Cancer Cell ◽  
Boronic Acid ◽  
Inductively Coupled Plasma ◽  
Normal Cell ◽  
Sialic Acids ◽  
Inductively Coupled ◽  
Plasma Mass Spectrometry

Sialic acids are special sugars widely expressed at the termini of glycan chains on the cell surface, and their expression level on the cancer cell surface is much higher than on the normal cell surface.

scholarly journals The Role of Sialic Acids in the Establishment of Infections by Pathogens, With Special Focus on Leishmania

2021 ◽  
Vol 11 ◽  
Author(s):  
Tainá Cavalcante ◽  
Mariana Medina Medeiros ◽  
Simon Ngao Mule ◽  
Giuseppe Palmisano ◽  
Beatriz Simonsen Stolf
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Host Cell ◽  
Functional Diversity ◽  
Sialic Acids ◽  
Cellular Communication ◽  
Special Focus ◽  
Functional Studies ◽  
Sialic Acid Binding

Carbohydrates or glycans are ubiquitous components of the cell surface which play crucial biological and structural roles. Sialic acids (Sias) are nine-carbon atoms sugars usually present as terminal residues of glycoproteins and glycolipids on the cell surface or secreted. They have important roles in cellular communication and also in infection and survival of pathogens. More than 20 pathogens can synthesize or capture Sias from their hosts and incorporate them into their own glycoconjugates and derivatives. Sialylation of pathogens’ glycoconjugates may be crucial for survival inside the host for numerous reasons. The role of Sias in protozoa such as Trypanosoma and Leishmania was demonstrated in previous studies. This review highlights the importance of Sias in several pathogenic infections, focusing on Leishmania. We describe in detail the contributions of Sias, Siglecs (sialic acid binding Ig-like lectins) and Neuraminidase 1 (NEU 1) in the course of Leishmania infection. A detailed view on the structural and functional diversity of Leishmania-related Sias and host-cell receptors will be provided, as well as the results of functional studies performed with different Leishmania species.

The Effect of Neuraminidase (3:2:1:18) on the Aggregation of Cells Dissociated from Embryonic Chick Muscle Tissue

1970 ◽  
Vol 6 (3) ◽  
pp. 751-766
Author(s):  
R. B. KEMP
Keyword(s):  
Cell Surface ◽  
Muscle Tissue ◽  
Muscle Cells ◽  
Cell Aggregation ◽  
Inhibitory Effect ◽  
Sialic Acids ◽  
Embryonic Chick ◽  
Experimental Conditions ◽  
Cell Counts

Embryonic chick muscle cells were used to investigate the effect of removing cell-surface sialic acids on cell aggregation in vitro. Single cell suspensions were prepared by dissociating skeletal muscle tissue of 9-day-old chick embryos with either crystalline or crude trypsin. Cell aggregation was quantitatively estimated by turbidimetric and gyratory shaker methods. Cells dissociated with crude trypsin and suspended in Hanks's balanced salts solution (BSS) containing 25u./ml neuraminidase (NANase) only aggregated for 2h when rotated in an absorptiometer. The inhibitory effect of the enzyme was more pronounced with increasing concentration up to 25u./ml. Cells dissociated with crystalline trypsin and treated with 100u./ml NANase immediately exhibited a reduced aggregative competence when gyrated in Eagle's minimum essential medium (MEM) containing 25u./ml NANase, compared with the controls which were not exposed to NANase. The aggregation rate of muscle cells pretreated with 100u./ml NANase and suspended in Eagle's MEM was similar to that of the untreated controls. Cell counts showed that under all three experimental conditions cells were not added to aggregates after the 12-h stage. Aggregates formed in Eagle's MEM (the controls) joined together to form larger aggregates after 12 h, but those rotating in the presence of NANase did not display this property. Lissamine green viability tests showed that cells remained alive throughout the 24-h period in the presence of NANase. Determinations of oxygen uptake, protein synthesis and mitotic index confirmed that general cellular viability was not affected by NANase. Fluorescent-labelled NANase was not taken up by the cells. Treatment of crystalline trypsin-dissociated muscle cells with 100u./ml NANase for 30 min at 37°C significantly reduced their negative electrophoretic mobility. This diminution closely corresponded to the removal of cell-surface sialic acids, as measured by colorimetric tests. Interpretation of the results in the light of current theories of cell adhesion failed to give support to the concept of adhesion by physical forces. The mechanism by which cellular deformability could influence cellular adhesiveness is modified in the knowledge of the present results.

A thin hydrogel barrier linked onto cell surface sialic acids through covalent bonds induces cancer cell death in vivo

2020 ◽  
Vol 8 (2) ◽  
pp. 577-585 ◽  
Author(s):  
Kimika Ono ◽  
Yuka Sanada ◽  
Yuka Kimura ◽  
Seika Aoyama ◽  
Natsumi Ueda ◽  
...  
Keyword(s):  
Cell Death ◽  
Sialic Acid ◽  
Cell Surface ◽  
Cancer Cell ◽  
Sialic Acids ◽  
Cell Surfaces ◽  
Covalent Bonds ◽  
Novel Technique ◽  
Cancer Cell Death

A novel technique to form a thin hydrogel barrier on aberrantly expressed sialic acid residues on cancer cell surfaces was developed.

scholarly journals An efficient and robust HPLC method to determine the sialylation levels of human epithelial cells

2021 ◽  
Author(s):  
Hyo Jeong Kim ◽  
Stephanie Schweiker ◽  
Katie Powell ◽  
Stephan Levonis
Keyword(s):  
Sialic Acid ◽  
Cell Surface ◽  
Flow Rate ◽  
Deoxycholic Acid ◽  
Ion Pairing ◽  
Hplc Method ◽  
Sialic Acids ◽  
Reverse Phase ◽  
Simple Method ◽  
Cell Matrix

Sialyltransferase, an enzyme responsible for attaching sialic acid to the cell surface, is reported to play a key role in cancer, making sialyltransferase a potent therapeutic target in drug development for cancer. Hence, this paper aimed to develop a simple method to detect and quantify sialic acids in cancer cells. An efficient method was developed using a reverse-phase ion-pairing HPLC-UV using triisopropanolamine as the ion-pairing agent with a C18 column. Neu5Ac was successfully eluted with the retention time 6.344 min with a flow rate of 0.4 mL/min. The proposed method was validated appropriately according to the AOAC guidelines (2013). This work demonstrates that the proposed method is not only relatively simple but also cost and time effective compared to pre-existing methods to successfully determine both free and protein-bound Neu5Ac in a complex cancer cell matrix. Furthermore, by applying the proposed method, a statistically significant decrease was observed for both HeLa and HuCCT1 cell lines with the application of deoxycholic acid – a known sialyltransferase inhibitor. Hence, the proposed method may be applicable to evaluate the effectiveness of sialyltransferase inhibitors.

scholarly journals ST6GAL1-mediated heterogeneity in sialic acid levels potentiates invasion of breast cancer epithelia

2020 ◽  
Author(s):  
Dharma Pally ◽  
Durjay Pramanik ◽  
Shahid Hussain ◽  
Shreya Verma ◽  
Anagha Srinivas ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Sialic Acid ◽  
Cell Surface ◽  
Single Cells ◽  
Computational Modelling ◽  
Cancer Cell Line ◽  
Sialic Acids ◽  
Cellular Potts Model ◽  
Experimental Findings

AbstractHeterogeneity in phenotypes of malignantly transformed cells and aberrant glycan expression on their surface are two prominent hallmarks of cancers that have hitherto not been linked to each other. In this paper, we identify heterogeneity in a specific glycan linkage: α2,6-linked sialic acids within breast cancer cells in vivo and in culture. Upon sorting out two populations with moderate and relatively higher cell surface α2,6-linked sialic acid levels from the triple negative breast cancer cell line MDA-MB-231, both populations (denoted as medium and high-2,6-Sial cells respectively) stably retained their levels in early passages. Upon continuous culturing, medium 2,6-Sial cells recapitulated the heterogeneity of the unsorted line whereas high 2,6-Sial cells showed no such tendency. Compared with the high 2,6-Sial, the medium 2,6-Sial cells showed greater adhesion to reconstituted extracellular matrices (ECM) as well as invaded faster as single cells. The level of α2,6-linked sialic acids in the two sublines was found to be consistent with the expression of a specific glycosyl transferase, ST6GAL1. Stably knocking down ST6GAL1 in the high 2,6-Sial cells, enhanced their invasiveness. When cultured together, medium 2,6-Sial cells differentially migrated to the edge of growing tumoroid-like cultures, whereas high 2,6-Sial cells formed the central bulk. Simulations in a Cellular Potts model-based computational environment that is calibrated to our experimental findings suggest that the heterogeneity of cell-ECM adhesion, likely regulated by α2,6-linked sialic acids facilitates niches of highly invasive cells to efficiently migrate centrifugally as the invasive front of a malignant tumor.Significance StatementCell-surface sugars are aberrantly expressed in cancer but their contributions to tumor heterogeneity are not known. In this study, we uncover and separate breast cancer populations with distinct α2,6-linked sialic acid levels. The moderately expressing population shows stronger adhesion to extracellular matrix than the high expressing population. It also invades faster through the matrix as single cells. Combining experiments with computational modelling, we show that the heterogeneity in matrix adhesion is vital to accentuating cell invasion. In some conditions, invasion of heterogeneous populations may compare with, or exceed that of, homogeneous moderately expressing populations. Our findings are vital to furthering our understanding of how cancers spread and potentially qualify efforts to manage the disease through glycan-editing or immunotherapeutic approaches.

scholarly journals Structural Basis and Evolution of Glycan Receptor Specificities within the Polyomavirus Family

mBio ◽  
2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Luisa J. Ströh ◽  
Nils H. Rustmeier ◽  
Bärbel S. Blaum ◽  
Josephine Botsch ◽  
Philip Rößler ◽  
...  
Keyword(s):  
New Jersey ◽  
Sialic Acid ◽  
Cell Surface ◽  
Binding Site ◽  
Receptor Binding ◽  
Sialic Acids ◽  
Human Polyomavirus ◽  
Organ Transplant Recipient ◽  
Host Switching ◽  
Sialic Acid Binding

ABSTRACT Asymptomatic infections with polyomaviruses in humans are common, but these small viruses can cause severe diseases in immunocompromised hosts. New Jersey polyomavirus (NJPyV) was identified via a muscle biopsy in an organ transplant recipient with systemic vasculitis, myositis, and retinal blindness, and human polyomavirus 12 (HPyV12) was detected in human liver tissue. The evolutionary origins and potential diseases are not well understood for either virus. In order to define their receptor engagement strategies, we first used nuclear magnetic resonance (NMR) spectroscopy to establish that the major capsid proteins (VP1) of both viruses bind to sialic acid in solution. We then solved crystal structures of NJPyV and HPyV12 VP1 alone and in complex with sialylated glycans. NJPyV employs a novel binding site for a α2,3-linked sialic acid, whereas HPyV12 engages terminal α2,3- or α2,6-linked sialic acids in an exposed site similar to that found in Trichodysplasia spinulosa-associated polyomavirus (TSPyV). Gangliosides or glycoproteins, featuring in mammals usually terminal sialic acids, are therefore receptor candidates for both viruses. Structural analyses show that the sialic acid-binding site of NJPyV is conserved in chimpanzee polyomavirus (ChPyV) and that the sialic acid-binding site of HPyV12 is widely used across the entire polyomavirus family, including mammalian and avian polyomaviruses. A comparison with other polyomavirus-receptor complex structures shows that their capsids have evolved to generate several physically distinct virus-specific receptor-binding sites that can all specifically engage sialylated glycans through a limited number of contacts. Small changes in each site may have enabled host-switching events during the evolution of polyomaviruses. IMPORTANCE Virus attachment to cell surface receptors is critical for productive infection. In this study, we have used a structure-based approach to investigate the cell surface recognition event for New Jersey polyomavirus (NJPyV) and human polyomavirus 12 (HPyV12). These viruses belong to the polyomavirus family, whose members target different tissues and hosts, including mammals, birds, fish, and invertebrates. Polyomaviruses are nonenveloped viruses, and the receptor-binding site is located in their capsid protein VP1. The NJPyV capsid features a novel sialic acid-binding site that is shifted in comparison to other structurally characterized polyomaviruses but shared with a closely related simian virus. In contrast, HPyV12 VP1 engages terminal sialic acids in a manner similar to the human Trichodysplasia spinulosa-associated polyomavirus. Our structure-based phylogenetic analysis highlights that even distantly related avian polyomaviruses possess the same exposed sialic acid-binding site. These findings complement phylogenetic models of host-virus codivergence and may also reflect past host-switching events.

The effects of surfactants on cell aggregation

1978 ◽  
Vol 32 (1) ◽  
pp. 363-376
Author(s):  
E. Owen ◽  
J. Clifford ◽  
A. Marson
Keyword(s):  
Sialic Acid ◽  
Ionic Strength ◽  
Cell Membrane ◽  
Cell Surface ◽  
Surfactant Concentration ◽  
Cell Aggregation ◽  
Ionic Surfactant ◽  
Human Amnion ◽  
Cell Surface Glycoproteins ◽  
Effects Of Temperature

Trypsin-dissociated HeLa and human amnion cells were employed to investigate the effects of an anionic, a cationic, and a non-ionic surfactant on cell reaggregation. All the surfactants inhibited the reaggregation process, the effect increasing with surfactant concentration, and becoming significant at concentrations of about 10(−6) M for the anionic surfactant and about 10(−5) M for the others. The effects of temperature and ionic strength on HeLa cell aggregation, and of surfactants on the electrophoretic mobility of HeLa cells and the release of sialic acid from their surfaces by neuraminidase, were also examined. The results indicate that although electrostatic effects occur and are likely to be of importance in cell reaggregation, the effect of surfactants cannot be accounted for on this basis alone, and it is suggested that interactions involving the cell-surface glycoproteins, possibly indirectly via effects on the fluidity of the cell membrane, are also significant in this respect.

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