Mast cell adhesion induces cytoskeletal modifications and programmed cell death in oligodendrocytes

2010 ◽  
Vol 218 (1-2) ◽  
pp. 57-66 ◽  
Author(s):  
Nevenka Medic ◽  
Paola Lorenzon ◽  
Francesca Vita ◽  
Elisa Trevisan ◽  
Anna Marchioli ◽  
...  
Keyword(s):  
Cell Death ◽  
Mast Cell ◽  
Cell Adhesion ◽  
Programmed Cell Death

scholarly journals A Screen for Mutations That Suppress the Phenotype of Drosophila armadillo, the β-Catenin Homolog

Genetics ◽  
2000 ◽  
Vol 155 (4) ◽  
pp. 1725-1740
Author(s):  
Rachel T Cox ◽  
Donald G McEwen ◽  
Denise L Myster ◽  
Robert J Duronio ◽  
Joseph Loureiro ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
Programmed Cell Death ◽  
Cell Survival ◽  
Wnt Pathway ◽  
Genetic Modifier ◽  
Wnt Signaling Pathway ◽  
Adherens Junction ◽  
Cell Fates ◽  
Wnt Signal

Abstract During development signaling pathways coordinate cell fates and regulate the choice between cell survival or programmed cell death. The well-conserved Wingless/Wnt pathway is required for many developmental decisions in all animals. One transducer of the Wingless/Wnt signal is Armadillo/β-catenin. Drosophila Armadillo not only transduces Wingless signal, but also acts in cell-cell adhesion via its role in the epithelial adherens junction. While many components of both the Wingless/Wnt signaling pathway and adherens junctions are known, both processes are complex, suggesting that unknown components influence signaling and junctions. We carried out a genetic modifier screen to identify some of these components by screening for mutations that can suppress the armadillo mutant phenotype. We identified 12 regions of the genome that have this property. From these regions and from additional candidate genes tested we identified four genes that suppress arm: dTCF, puckered, head involution defective (hid), and Dpresenilin. We further investigated the interaction with hid, a known regulator of programmed cell death. Our data suggest that Wg signaling modulates Hid activity and that Hid regulates programmed cell death in a dose-sensitive fashion.

scholarly journals Effect of Thermal Stimulation on Gene Expression Related to Skeletal Muscle-derived Cell Density

2021 ◽  
pp. 73-81
Author(s):  
Masayo Nagai ◽  
Hidesuke Kaji
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Cell Death ◽  
Cell Adhesion ◽  
Cell Growth ◽  
Programmed Cell Death ◽  
Mrna Expression ◽  
Thermal Stimulation ◽  
Heat Stimulation ◽  
Stimulation Of

Aims: Our previous study demonstrated favorable changes in plasma protein levels such as adiponectin by fomentation in healthy people. We also reported that the thermal stimulation caused changes of mRNA levels to prevent atherosclerosis in human skeletal muscle-derived cell (SMDC). However, cell number decreased to 74.6% by heat stimulation. In order to clarify this mechanism, we investigated whether the heat stimulation affects the levels of mRNA related to cell density or number of SMDC. Study Design: Experimental study comparing transcriptome between cells cultured at higher temperature and control cells. Place and Duration of Study: From September 2015 to March 2017, Division of Physiology and Metabolism, University of Hyogo. Methodology: SMDC was cultured at 42°C and 37°C and its gene expression was analyzed by using microarray technique. Results: Thermal stimulation of SMDC significantly altered the expression of 10 genes related to apoptosis, 1 gene related to cell division and 1 gene related to cell adhesion. mRNA expression of apoptosis promoting gene, such as THAP2 (THAP domain containing, apoptosis associated protein 2), PDCD6 (programmed cell death 6), BCL2L13 (BCL2-like 13), LOC728613 (programmed cell death 6 pseudogene), CASP4 (caspase 4), and FAS (Fas cell surface death, receptor) was up-regulated. On the other hand, PAWR (PRKC, apoptosis, WT1, regulator) was downregulated, and mRNA expression of anti-apoptotic genes, such as NOL3 (nucleolar protein 3), CIAPIN1 (cytokine-induced apoptosis inhibitor 1) and NAIF1 (nuclear apoptosis inducing factor1), was up-regulated, Gene Ontology analysis showed alterations in the expression of genes that promote apoptosis and cell growth inhibition. Pathway analysis demonstrated the pathways that promote apoptosis, stimulate cell growth and negatively or positively regulate cell adhesion. Conclusion: The present study suggested that thermal stimulation of SMDC might predominantly promote apoptosis from consistent changes in related gene expression by any analysis.

scholarly journals Interplay in neural functions of cell adhesion molecule close homolog of L1 (CHL1) and Programmed Cell Death 6 (PDCD6)

2021 ◽  
Author(s):  
Gabriele Loers ◽  
Thomas Theis ◽  
Helen Baixia Hao ◽  
Ralf Kleene ◽  
Sanjana Arsha ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Adhesion ◽  
Programmed Cell Death ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Close Homolog

Programmed Cell Death Ligand 1 and Venous Thromboembolism in Patients with Primary Brain Tumors

2019 ◽  
Author(s):  
P. Seyed Mir ◽  
A.-S. Berghoff ◽  
M. Preusser ◽  
G. Ricken ◽  
J. Riedl ◽  
...  
Keyword(s):  
Cell Death ◽  
Venous Thromboembolism ◽  
Programmed Cell Death ◽  
Brain Tumors ◽  
Primary Brain Tumors

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

Dynamical analysis of the programmed cell death pathway

2007 ◽  
Author(s):  
Luciano Carotenuto ◽  
Vincenza Pace ◽  
Dina Bellizzi ◽  
Giovanna De Benedictis
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dynamical Analysis ◽  
Cell Death Pathway

Biological response of the organism to the introduction of metal nanocomposites

2020 ◽  
pp. 761-762
Author(s):  
L. M. Sosedova ◽  
V. S. Rukavishnikov ◽  
E. A. Titov
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Biological Response ◽  
Brain Cell ◽  
Metal Nanocomposites ◽  
The Brain

The results of a study on rats toxicity of nanoparticles of metals bismuth, gadolinium and silver encapsulated in a natural biopolymer matrix arabinogalactan are presented. When intake of nanocomposite of silver revealed the readiness of the brain cell to apoptosis. The effect of bismuth and gadolinium nanocomposites did not cause an increase in the process of programmed cell death.

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