scholarly journals Time resolved study of cell death mechanisms induced by amine-modified polystyrene nanoparticles

Nanoscale ◽  
2013 ◽  
Vol 5 (22) ◽  
pp. 10868 ◽  
Author(s):  
Fengjuan Wang ◽  
Mariana G. Bexiga ◽  
Sergio Anguissola ◽  
Patricia Boya ◽  
Jeremy C. Simpson ◽  
...  
Keyword(s):  
Cell Death ◽  
Polystyrene Nanoparticles ◽  
Time Resolved ◽  
Cell Death Mechanisms ◽  
Modified Polystyrene

scholarly journals Time-resolved characterization of the mechanisms of toxicity induced by silica and amino-modified polystyrene on alveolar-like macrophages

2019 ◽  
Vol 94 (1) ◽  
pp. 173-186 ◽  
Author(s):  
Sarah Deville ◽  
Birgit Honrath ◽  
Quynh T. D. Tran ◽  
Gyorgy Fejer ◽  
Ivo Lambrichts ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Types ◽  
Similar Time ◽  
Time Resolved ◽  
Membrane Hyperpolarization ◽  
Mechanisms Of Toxicity ◽  
Cellular Reactive Oxygen Species ◽  
Foreign Materials ◽  
Modified Polystyrene ◽  
Different Cell Types

Abstract Macrophages play a major role in the removal of foreign materials, including nano-sized materials, such as nanomedicines and other nanoparticles, which they accumulate very efficiently. Because of this, it is recognized that for a safe development of nanotechnologies and nanomedicine, it is essential to investigate potential effects induced by nano-sized materials on macrophages. To this aim, in this work, a recently established model of primary murine alveolar-like macrophages was used to investigate macrophage responses to two well-known nanoparticle models: 50 nm amino-modified polystyrene, known to induce cell death via lysosomal damage and apoptosis in different cell types, and 50 nm silica nanoparticles, which are generally considered non-toxic. Then, a time-resolved study was performed to characterize in detail the response of the macrophages following exposure to the two nanoparticles. As expected, exposure to the amino-modified polystyrene led to cell death, but surprisingly no lysosomal swelling or apoptosis were detected. On the contrary, a peculiar mitochondrial membrane hyperpolarization was observed, accompanied by endoplasmic reticulum stress (ER stress), increased cellular reactive oxygen species (ROS) and changes of metabolic activity, ultimately leading to cell death. Strong toxic responses were observed also after exposure to silica, which included mitochondrial ROS production, mitochondrial depolarization and cell death by apoptosis. Overall, these results showed that exposure to the two nanoparticles led to a very different series of intracellular events, suggesting that the macrophages responded differently to the two nanoparticle models. Similar time-resolved studies are required to characterize the response of macrophages to nanoparticles, as a key parameter in nanosafety assessment.

scholarly journals Lysosome-dependent cell death and deregulated autophagy induced by amine-modified polystyrene nanoparticles

Open Biology ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 170271 ◽  
Author(s):  
Fengjuan Wang ◽  
Anna Salvati ◽  
Patricia Boya
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Fibroblast Cell ◽  
Mouse Embryonic Fibroblast ◽  
Autophagic Flux ◽  
Polystyrene Nanoparticles ◽  
Dependent Cell ◽  
Modified Polystyrene ◽  
Embryonic Fibroblast ◽  
1321N1 Cell

Nanoparticles (NPs) typically accumulate in lysosomes. However, their impact on lysosomal function, as well as autophagy, a lysosomal degradative pathway, is still not well known. We have previously reported in the 1321N1 cell line that amine-modified polystyrene (NH 2 -PS) NPs induce apoptosis through damage initiated in the lysosomes leading ultimately to release of lysosomal content in the cytosol, followed by apoptosis. Here, by using a combination of biochemical and cell biological approaches, we have characterized in a mouse embryonic fibroblast cell line that the lysosomal alterations induced by NH 2 -PS NPs is progressive, initiating from mild lysosomal membrane permeabilization (LMP), to expansion of lysosomal volume and intensive LMP before the summit of cell death. Though the cells initially seem to induce autophagy as a surviving mechanism, the damage of NH 2 -PS NPs to lysosomes probably results in lysosomal dysfunctions, leading to blockage of autophagic flux at the level of lysosomes and the eventual cell death.

Different cell death mechanisms are triggered by acute or chronic right heart failure-induced liver failure

2011 ◽  
Vol 49 (01) ◽  
Author(s):  
K Herzer ◽  
G Kneiseler ◽  
F Post ◽  
M Schlattjan ◽  
T Neumann ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Liver Failure ◽  
Right Heart Failure ◽  
Right Heart ◽  
Cell Death Mechanisms

EFFECT OF COLCHICINE AND ATORVASTATIN ON CELL DEATH MECHANISMS DURING INFLAMMATORY PROCESSES IN ATHEROSCHLEROSIS

2018 ◽  
Vol 74 (11) ◽  
Author(s):  
Gunnur Demircan ◽  
Sule Beyhan Ozdas ◽  
Demet Akin ◽  
Ozgur Kaplan ◽  
Sabri Demircan ◽  
...  
Keyword(s):  
Cell Death ◽  
Inflammatory Processes ◽  
Cell Death Mechanisms

Cytotoxicity and Cell Death Mechanisms Induced by a Novel Bisnaphthalimidopropyl Derivative against the NCI-H460 non-small Lung Cancer Cell Line

2013 ◽  
Vol 13 (3) ◽  
pp. 414-421 ◽  
Author(s):  
Raquel T. Lima ◽  
Gemma A. Barron ◽  
Joanna A. Grabowska ◽  
Giovanna Bermano ◽  
Simranjeet Kaur ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cell ◽  
Cell Death Mechanisms

Organelle Stress Sensors and Cell Death Mechanisms in Neurodegenerative Diseases

2010 ◽  
Vol 9 (6) ◽  
pp. 679-692 ◽  
Author(s):  
Ricardo J.S. Viana ◽  
Maria B. Fonseca ◽  
Rita M. Ramalho ◽  
Ana F. Nunes ◽  
Cecilia M.P. Rodrigues
Keyword(s):  
Cell Death ◽  
Neurodegenerative Diseases ◽  
Stress Sensors ◽  
Cell Death Mechanisms

scholarly journals Suppressing Pyroptosis Augments Post-Transplant Survival of Stem Cells and Cardiac Function Following Ischemic Injury

2021 ◽  
Vol 22 (15) ◽  
pp. 7946
Author(s):  
Chang Youn Lee ◽  
Seahyoung Lee ◽  
Seongtae Jeong ◽  
Jiyun Lee ◽  
Hyang-Hee Seo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Death ◽  
Stem Cell ◽  
Cardiac Fibrosis ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Transplant Survival ◽  
Post Transplant ◽  
Heart Functions ◽  
Cell Death Mechanisms

The acute demise of stem cells following transplantation significantly compromises the efficacy of stem cell-based cell therapeutics for infarcted hearts. As the stem cells transplanted into the damaged heart are readily exposed to the hostile environment, it can be assumed that the acute death of the transplanted stem cells is also inflicted by the same environmental cues that caused massive death of the host cardiac cells. Pyroptosis, a highly inflammatory form of programmed cell death, has been added to the list of important cell death mechanisms in the damaged heart. However, unlike the well-established cell death mechanisms such as necrosis or apoptosis, the exact role and significance of pyroptosis in the acute death of transplanted stem cells have not been explored in depth. In the present study, we found that M1 macrophages mediate the pyroptosis in the ischemia/reperfusion (I/R) injured hearts and identified miRNA-762 as an important regulator of interleukin 1b production and subsequent pyroptosis. Delivery of exogenous miRNA-762 prior to transplantation significantly increased the post-transplant survival of stem cells and also significantly ameliorated cardiac fibrosis and heart functions following I/R injury. Our data strongly suggest that suppressing pyroptosis can be an effective adjuvant strategy to enhance the efficacy of stem cell-based therapeutics for diseased hearts.

scholarly journals Mitochondrion-Dependent Cell Death in TDP-43 Proteinopathies

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 376
Author(s):  
Chantal B. Lucini ◽  
Ralf J. Braun
Keyword(s):  
Cell Death ◽  
Oxygen Species ◽  
In Vivo Models ◽  
Dependent Cell ◽  
Cell Death Mechanisms ◽  
Sting Pathway ◽  
Mitochondrial Membrane Permeabilization

In the last decade, pieces of evidence for TDP-43-mediated mitochondrial dysfunction in neurodegenerative diseases have accumulated. In patient samples, in vitro and in vivo models have shown mitochondrial accumulation of TDP-43, concomitantly with hallmarks of mitochondrial destabilization, such as increased production of reactive oxygen species (ROS), reduced level of oxidative phosphorylation (OXPHOS), and mitochondrial membrane permeabilization. Incidences of TDP-43-dependent cell death, which depends on mitochondrial DNA (mtDNA) content, is increased upon ageing. However, the molecular pathways behind mitochondrion-dependent cell death in TDP-43 proteinopathies remained unclear. In this review, we discuss the role of TDP-43 in mitochondria, as well as in mitochondrion-dependent cell death. This review includes the recent discovery of the TDP-43-dependent activation of the innate immunity cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) pathway. Unravelling cell death mechanisms upon TDP-43 accumulation in mitochondria may open up new opportunities in TDP-43 proteinopathy research.

scholarly journals Cell Death in Coronavirus Infections: Uncovering Its Role during COVID-19

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1585
Author(s):  
Annamaria Paolini ◽  
Rebecca Borella ◽  
Sara De Biasi ◽  
Anita Neroni ◽  
Marco Mattioli ◽  
...  
Keyword(s):  
Cell Death ◽  
Immune Cells ◽  
Viral Infections ◽  
Virus Entry ◽  
Therapeutic Strategies ◽  
The Other ◽  
Cytokine Storm ◽  
Cytokines And Chemokines ◽  
Cell Death Mechanisms ◽  
The One

Cell death mechanisms are crucial to maintain an appropriate environment for the functionality of healthy cells. However, during viral infections, dysregulation of these processes can be present and can participate in the pathogenetic mechanisms of the disease. In this review, we describe some features of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and some immunopathogenic mechanisms characterizing the present coronavirus disease (COVID-19). Lymphopenia and monocytopenia are important contributors to COVID-19 immunopathogenesis. The fine mechanisms underlying these phenomena are still unknown, and several hypotheses have been raised, some of which assign a role to cell death as far as the reduction of specific types of immune cells is concerned. Thus, we discuss three major pathways such as apoptosis, necroptosis, and pyroptosis, and suggest that all of them likely occur simultaneously in COVID-19 patients. We describe that SARS-CoV-2 can have both a direct and an indirect role in inducing cell death. Indeed, on the one hand, cell death can be caused by the virus entry into cells, on the other, the excessive concentration of cytokines and chemokines, a process that is known as a COVID-19-related cytokine storm, exerts deleterious effects on circulating immune cells. However, the overall knowledge of these mechanisms is still scarce and further studies are needed to delineate new therapeutic strategies.

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