scholarly journals Gallic Acid Triggers Iron-Dependent Cell Death with Apoptotic, Ferroptotic, and Necroptotic Features

Toxins ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 492 ◽  
Author(s):  
Ho Man Tang ◽  
Peter Chi Keung Cheung
Keyword(s):  
Cell Death ◽  
Gallic Acid ◽  
Fruits And Vegetables ◽  
Membrane Integrity ◽  
Food Sources ◽  
Death Process ◽  
Cytochrome C Release ◽  
Anti Cancer ◽  
Cell Death Process ◽  
Dependent Cell

Gallic acid (GA) is a natural anti-cancer compound that can be found in many food sources, including edible mushrooms, fruits, and vegetables. Studies generally attribute the anti-cancer activity of GA to the induction of apoptosis. Here, we reported that GA activated iron-dependent cell death mechanisms with apoptotic, ferroptotic, and necroptotic features. Our time-lapse live-cell microscopy study demonstrated that GA could induce coexistence of multiple types of cell death pathways, including apoptosis characterized by mitochondrial cytochrome c release and caspase-3 activation, ferroptosis characterized by lipid peroxidation, and necroptosis characterized by the loss of plasma membrane integrity. This GA-induced cell death could be completely suppressed by exposure to an iron chelator deferoxamine, indicating that it is an iron-dependent cell death process. Importantly, MLKL (mixed lineage kinase domain-like protein) inhibitor necrosulfonamide exerted a synergistic effect by increasing the sensitivity of cancer cells to GA. Taken together, our results provide new mechanistic insights, and also suggest new strategies to enhance the efficacy of this natural anti-cancer compound by identifying the agents that can promote or suppress the GA-induced cell death process.

scholarly journals Gene expression profile analysis of gallic acid-induced cell death process

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ho Man Tang ◽  
Peter Chi Keung Cheung
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Gallic Acid ◽  
Time Course ◽  
Early Stage ◽  
Expression Profiles ◽  
Death Process ◽  
Apoptotic Pathway ◽  
Cell Death Pathway ◽  
Cell Death Process

AbstractGallic acid is a natural phenolic compound that displays anti-cancer properties in clinically relevant cell culture and rodent models. To date, the molecular mechanism governing the gallic acid-induced cancer cell death process is largely unclear, thus hindering development of novel therapeutics. Therefore, we performed time-course RNA-sequencing to reveal the gene expression profiles at the early (2nd hour), middle (4th and 6th hour), and late (9th hour) stages of the gallic acid-induced cell death process in HeLa cells. By Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, we found significant changes in transcription of the genes in different types of cell death pathways. This involved the ferroptotic cell death pathway at the early stage, apoptotic pathway at the middle stage, and necroptotic pathway at the late stage. Metabolic pathways were identified at all the stages, indicating that this is an active cell death process. Interestingly, the initiation and execution of gallic acid-induced cell death were mediated by multiple biological processes, including iron and amino acid metabolism, and the biosynthesis of glutathione, as targeting on these pathways suppressed cell death. In summary, our work provides a dataset with differentially expressed genes across different stages of cell death process during the gallic acid induction, which is important for further study on the control of this cell death mechanism.

NEURODEGENERATION PROCESSES GO FAR BEYOND NECROSIS AND APOPTOSIS!

2021 ◽  
Vol 1 (1) ◽  
pp. 1-19
Author(s):  
Rogério De Freitas Lacerda ◽  
Abigail Gonçalves da Silva ◽  
Isabela Cristina Sena Romano
Keyword(s):  
Cell Death ◽  
Neural Plasticity ◽  
Neuronal Cell Death ◽  
Morphological Characteristics ◽  
Neuronal Cell ◽  
Death Process ◽  
Molecular Systems ◽  
Cell Death Process ◽  
Dependent Cell ◽  
Apoptosis And Necrosis

Neural plasticity is a consequence of a delicate balance between the processes of neurodegeneration and neurogenesis. When neurodegeneration overcomes neurogenesis, neurodegenerative diseases occur, which affect cognitive functions such as memory, language, and executive functions. Neurodegeneration, the process of neuronal cell death, presents several aspects that were categorized according to their macroscopic and/or morphological characteristics. The concept of apoptosis, autophagy, and necrosis is still widely used today. On the other hand, more in-depth forms emerge in the clinical and academia, describing the cascade of cell death events through biochemical approaches, and the essential (causal) and accessory (correlative) aspects of the cell death process. New concepts were introduced, addressed in the modules of signal translation involving issues such as the initiation, execution, and propagation of cell death, as well as the pathophysiological relevance of each of the main types. Currently, twelve types of cell death are already defined, not only apoptosis, necrosis, and autophagy. In this review, we will address the main mechanisms of cell death, with special emphasis on the participation of caspases and other proteins in these mechanisms. We will discuss some types of cell death such as extrinsic and intrinsic apoptosis, necrosis, necroptosis, and autophagy-dependent cell death. We hope to elucidate key points in molecular systems, including the receptors involved in cell death and their role in neurodegeneration, and showing that neurodegeneration has characteristics beyond morphological (apoptosis and necrosis).

scholarly journals Correction: PML induces a novel caspase-independent cell death process

10.1038/8706 ◽  
1999 ◽  
Vol 22 (1) ◽  
pp. 115-115 ◽  
Author(s):  
Fredérique Quignon
Keyword(s):  
Cell Death ◽  
Death Process ◽  
Cell Death Process

scholarly journals Production of Prodiginines Is Part of a Programmed Cell Death Process in Streptomyces coelicolor

2018 ◽  
Vol 9 ◽  
Author(s):  
Elodie Tenconi ◽  
Matthew F. Traxler ◽  
Charline Hoebreck ◽  
Gilles P. van Wezel ◽  
Sébastien Rigali
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Streptomyces Coelicolor ◽  
Death Process ◽  
Cell Death Process

Characterization of cell death process in plant cells induced by hipoxia and anoxia

2000 ◽  
Vol 28 (5) ◽  
pp. A372-A372
Author(s):  
E. N. Baranova ◽  
N. V. Kononenko ◽  
T. V. Bragina ◽  
G. M. Grineva ◽  
T. P. Astafurova ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Cells ◽  
Death Process ◽  
Cell Death Process

Internucleosomal DNA fragmentation and programmed cell death (apoptosis) in the interdigital tissue of the embryonic chick leg bud

1993 ◽  
Vol 106 (1) ◽  
pp. 201-208 ◽  
Author(s):  
V. Garcia-Martinez ◽  
D. Macias ◽  
Y. Ganan ◽  
J.M. Garcia-Lobo ◽  
M.V. Francia ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Limb Development ◽  
Light Transmission ◽  
Morphological Changes ◽  
Death Process ◽  
Chondrogenic Potential ◽  
Cell Death Process ◽  
Dying Cells

In this work we have attempted to characterize the programmed cell death process in the chick embryonic interdigital tissue. Interdigital cell death is a prominent phenomenon during limb development and has the role of sculpturing the digits. Morphological changes in the regressing interdigital tissue studied by light, transmission and scanning electron microscopy were correlated with the occurrence of internucleosomal DNA fragmentation, evaluated using agarose gels. Programming of the cell death process was also analyzed by testing the chondrogenic potential of the interdigital mesenchyme, in high density cultures. Our results reveal a progressive loss of the chondrogenic potential of the interdigital mesenchyme, detectable 36 hours before the onset of the degenerative process. Internucleosomal DNA fragmentation was only detected concomitant with the appearance of cells dying with the morphology of apoptosis, but unspecific DNA fragmentation was also present at the same time. This unspecific DNA fragmentation was explained by a precocious activation of the phagocytic removal of the dying cells, confirmed in the tissue sections. From our observations it is suggested that programming of cell death involves changes before endonuclease activation. Further, cell surface changes involved in the phagocytic uptake of the dying cells appear to be as precocious as endonuclease activation.

scholarly journals Oxidative Stress in Cell Death and Cardiovascular Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Tao Xu ◽  
Wei Ding ◽  
Xiaoyu Ji ◽  
Xiang Ao ◽  
Ying Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiovascular Diseases ◽  
Death Process ◽  
Ros Production ◽  
Disease Treatment ◽  
Physiological Conditions ◽  
Intracellular Ros ◽  
Cell Death Process ◽  
Molecular Components ◽  
Multiple Signaling

ROS functions as a second messenger and modulates multiple signaling pathways under the physiological conditions. However, excessive intracellular ROS causes damage to the molecular components of the cell, which promotes the pathogenesis of various human diseases. Cardiovascular diseases are serious threats to human health with extremely high rates of morbidity and mortality. Dysregulation of cell death promotes the pathogenesis of cardiovascular diseases and is the clinical target during the disease treatment. Numerous studies show that ROS production is closely linked to the cell death process and promotes the occurrence and development of the cardiovascular diseases. In this review, we summarize the regulation of intracellular ROS, the roles of ROS played in the development of cardiovascular diseases, and the programmed cell death induced by intracellular ROS. We also focus on anti-ROS system and the potential application of anti-ROS strategy in the treatment of cardiovascular diseases.

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