usEP Induce Regulated Cell Death Mechanisms

2021 ◽  
pp. 227-263
Author(s):  
Stephen J. Beebe
Keyword(s):  
Cell Death ◽  
Regulated Cell Death ◽  
Cell Death Mechanisms

Abstract P419: A Systematic Characterization of Brain Endothelial Cell Death in Intracerebral Hemorrhage

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Maulana Ikhsan ◽  
Marietta Zille
Keyword(s):  
Cell Death ◽  
Intracerebral Hemorrhage ◽  
Brain Tissue ◽  
Vascular Integrity ◽  
Regulated Cell Death ◽  
Injury Mechanisms ◽  
Endothelial Cell Death ◽  
Cell Death Mechanisms ◽  
Underlying Mechanisms

Introduction: Intracerebral hemorrhage (ICH) is a type of stroke caused by the loss of vascular integrity leading to bleeding within the brain tissue. Hematoma-derived factors cause secondary injury mechanisms such as cell death days to weeks after the event and in regions distant from the primary insult. Increasing evidence suggests that hemoglobin released by the hematoma is one of the major contributors to neuronal injury in ICH. To date, it is unclear whether brain endothelial cells (EC) are similarly vulnerable to hemolysis products and undergo regulated cell death. Hypothesis: We hypothesized that brain EC undergo multiple, different modes of cell death after ICH and that the underlying mechanisms are different compared to neurons. Methods: We systematically investigated cell death mechanisms in brain EC after exposure to the hemolysis product hemin. We used chemical inhibitors of apoptosis, autophagy, ferroptosis, necroptosis, and parthanatos and assessed biochemical markers of these cell death modes. Results: Brain EC viability was concentration-dependently decreased, starting at higher hemin concentrations than neurons. Treatment of EC with ferroptosis inhibitors protective against hemin toxicity in neurons and against ICH in vivo showed that only N-acetylcysteine and deferoxamine protected brain EC, while ferrostatin-1 and U0126 did not abrogate EC death. The autophagy inhibitor bafilomycin A1 also reduced EC death and hemin increased the expression of the autophagy marker LC3. While inhibitors against apoptosis and parthanatos were not effective, the necroptosis inhibitor GSK872 demonstrated a partial protective effect. Conclusions: Our data suggest that ICH induces different mechanisms of death in EC (ferroptosis and autophagy) compared to neurons (ferroptosis and necroptosis) and may thus warrant a combinatorial therapeutic approach. Further investigations in human and ovine ICH brain tissue are ongoing.

scholarly journals Guidelines for evaluating myocardial cell death

2019 ◽  
Vol 317 (5) ◽  
pp. H891-H922 ◽  
Author(s):  
Paras K. Mishra ◽  
Adriana Adameova ◽  
Joseph A. Hill ◽  
Christopher P. Baines ◽  
Peter M. Kang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Best Practices ◽  
Cardiac Remodeling ◽  
Myocardial Cell ◽  
Autophagic Cell Death ◽  
Multiple Forms ◽  
Regulated Cell Death ◽  
Fundamental Process ◽  
Cell Death Mechanisms

Cell death is a fundamental process in cardiac pathologies. Recent studies have revealed multiple forms of cell death, and several of them have been demonstrated to underlie adverse cardiac remodeling and heart failure. With the expansion in the area of myocardial cell death and increasing concerns over rigor and reproducibility, it is important and timely to set a guideline for the best practices of evaluating myocardial cell death. There are six major forms of regulated cell death observed in cardiac pathologies, namely apoptosis, necroptosis, mitochondrial-mediated necrosis, pyroptosis, ferroptosis, and autophagic cell death. In this article, we describe the best methods to identify, measure, and evaluate these modes of myocardial cell death. In addition, we discuss the limitations of currently practiced myocardial cell death mechanisms. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/guidelines-for-evaluating-myocardial-cell-death/ .

scholarly journals The Role of Neutrophil NETosis in Organ Injury: Novel Inflammatory Cell Death Mechanisms

Inflammation ◽  
2020 ◽  
Vol 43 (6) ◽  
pp. 2021-2032 ◽  
Author(s):  
Zhen Cahilog ◽  
Hailin Zhao ◽  
Lingzhi Wu ◽  
Azeem Alam ◽  
Shiori Eguchi ◽  
...  
Keyword(s):  
Cell Death ◽  
Organ Injury ◽  
Microbial Function ◽  
Regulated Cell Death ◽  
Therapeutic Measures ◽  
Unexplored Area ◽  
Decondensed Chromatin ◽  
Cell Death Mechanisms ◽  
The Brain

Abstract NETosis is a type of regulated cell death dependent on the formation of neutrophil extracellular traps (NET), where net-like structures of decondensed chromatin and proteases are produced by polymorphonuclear (PMN) granulocytes. These structures immobilise pathogens and restrict them with antimicrobial molecules, thus preventing their spread. Whilst NETs possess a fundamental anti-microbial function within the innate immune system under physiological circumstances, increasing evidence also indicates that NETosis occurs in the pathogenic process of other disease type, including but not limited to atherosclerosis, airway inflammation, Alzheimer’s and stroke. Here, we reviewed the role of NETosis in the development of organ injury, including injury to the brain, lung, heart, kidney, musculoskeletal system, gut and reproductive system, whilst therapeutic agents in blocking injuries induced by NETosis in its primitive stages were also discussed. This review provides novel insights into the involvement of NETosis in different organ injuries, and whilst potential therapeutic measures targeting NETosis remain a largely unexplored area, these warrant further investigation.

Abstract TMP32: Ischemic Stroke Causes Vascular Regression in Type-II Diabetic Male Rats: Potential Role of Regulated Cell Death Mechanisms

Stroke ◽  
2018 ◽  
Vol 49 (Suppl_1) ◽  
Author(s):  
Yasir Abdul ◽  
Weiguo Li ◽  
Rebecca Ward ◽  
Sherif Hafez ◽  
Mohammed Abdelsaid ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Potential Role ◽  
Male Rats ◽  
Type Ii ◽  
Regulated Cell Death ◽  
Cell Death Mechanisms

scholarly journals Autophagy Regulation and Photodynamic Therapy: Insights to Improve Outcomes of Cancer Treatment

2021 ◽  
Vol 10 ◽  
Author(s):  
Waleska K. Martins ◽  
Renata Belotto ◽  
Maryana N. Silva ◽  
Daniel Grasso ◽  
Maynne D. Suriani ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cancer Therapy ◽  
Cancer Treatment ◽  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Light Sources ◽  
Regulated Cell Death ◽  
Age Related ◽  
Cell Death Mechanisms

Cancer is considered an age-related disease that, over the next 10 years, will become the most prevalent health problem worldwide. Although cancer therapy has remarkably improved in the last few decades, novel treatment concepts are needed to defeat this disease. Photodynamic Therapy (PDT) signalize a pathway to treat and manage several types of cancer. Over the past three decades, new light sources and photosensitizers (PS) have been developed to be applied in PDT. Nevertheless, there is a lack of knowledge to explain the main biochemical routes needed to trigger regulated cell death mechanisms, affecting, considerably, the scope of the PDT. Although autophagy modulation is being raised as an interesting strategy to be used in cancer therapy, the main aspects referring to the autophagy role over cell succumbing PDT-photoinduced damage remain elusive. Several reports emphasize cytoprotective autophagy, as an ultimate attempt of cells to cope with the photo-induced stress and to survive. Moreover, other underlying molecular mechanisms that evoke PDT-resistance of tumor cells were considered. We reviewed the paradigm about the PDT-regulated cell death mechanisms that involve autophagic impairment or boosted activation. To comprise the autophagy-targeted PDT-protocols to treat cancer, it was underlined those that alleviate or intensify PDT-resistance of tumor cells. Thereby, this review provides insights into the mechanisms by which PDT can be used to modulate autophagy and emphasizes how this field represents a promising therapeutic strategy for cancer treatment.

scholarly journals The Role of Necroptosis: Biological Relevance and Its Involvement in Cancer

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 684
Author(s):  
Laura Della Torre ◽  
Angela Nebbioso ◽  
Hendrik G. Stunnenberg ◽  
Joost H. A. Martens ◽  
Vincenzo Carafa ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Fate ◽  
Intervention Strategy ◽  
Biological Relevance ◽  
Cellular Events ◽  
Regulated Cell Death ◽  
Independent Form ◽  
Cell Death Mechanisms ◽  
Cell Fate Control ◽  
Novel Therapeutic

Regulated cell death mechanisms are essential for the maintenance of cellular homeostasis. Evasion of cell death is one of the most important hallmarks of cancer. Necroptosis is a caspase independent form of regulated cell death, investigated as a novel therapeutic strategy to eradicate apoptosis resistant cancer cells. The process can be triggered by a variety of stimuli and is controlled by the activation of RIP kinases family as well as MLKL. The well-studied executor, RIPK1, is able to modulate key cellular events through the interaction with several proteins, acting as strategic crossroads of several molecular pathways. Little evidence is reported about its involvement in tumorigenesis. In this review, we summarize current studies on the biological relevance of necroptosis, its contradictory role in cancer and its function in cell fate control. Targeting necroptosis might be a novel therapeutic intervention strategy in anticancer therapies as a pharmacologically controllable event.

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
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