scholarly journals On the Evolutionary Conservation of the Cell Death Pathway: Mitochondrial Release of an Apoptosis-inducing Factor duringDictyostelium discoideum Cell Death

2001 ◽  
Vol 12 (10) ◽  
pp. 3016-3030 ◽  
Author(s):  
Damien Arnoult ◽  
Irène Tatischeff ◽  
Jérome Estaquier ◽  
Mathilde Girard ◽  
Franck Sureau ◽  
...  
Keyword(s):  
Cell Death ◽  
Transmembrane Potential ◽  
External Surface ◽  
Evolutionary Conservation ◽  
Free System ◽  
Cell Death Pathway ◽  
Effector Pathway ◽  
A Cell ◽  
Multicellular Organisms ◽  
Apoptosis Inducing Factor

Mitochondria play a pivotal role in apoptosis in multicellular organisms by releasing apoptogenic factors such as cytochromec that activate the caspases effector pathway, and apoptosis-inducing factor (AIF) that is involved in a caspase-independent cell death pathway. Here we report that cell death in the single-celled organism Dictyostelium discoideuminvolves early disruption of mitochondrial transmembrane potential (ΔΨm) that precedes the induction of several apoptosis-like features, including exposure of the phosphatidyl residues at the external surface of the plasma membrane, an intense vacuolization, a fragmentation of DNA into large fragments, an autophagy, and the release of apoptotic corpses that are engulfed by neighboring cells. We have cloned a Dictyostelium homolog of mammalian AIF that is localized into mitochondria and is translocated from the mitochondria to the cytoplasm and the nucleus after the onset of cell death. Cytoplasmic extracts from dying Dictyosteliumcells trigger the breakdown of isolated mammalian andDictyostelium nuclei in a cell-free system, and this process is inhibited by a polyclonal antibody specific forDictyostelium discoideum apoptosis-inducing factor (DdAIF), suggesting that DdAIF is involved in DNA degradation duringDictyostelium cell death. Our findings indicate that the cell death pathway in Dictyostelium involves mitochondria and an AIF homolog, suggesting the evolutionary conservation of at least part of the cell death pathway in unicellular and multicellular organisms.

Programmed cell death in African trypanosomes

Parasitology ◽  
2006 ◽  
Vol 132 (S1) ◽  
pp. S7-S18 ◽  
Author(s):  
S. C. WELBURN ◽  
E. MACLEOD ◽  
K. FIGARELLA ◽  
M. DUZENSKO
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Growth And Development ◽  
Parasitic Protozoa ◽  
African Trypanosomes ◽  
Cell Death Pathway ◽  
A Cell ◽  
Multicellular Organisms

Until recently it had generally been assumed that apoptosis and other forms of programmed cell death evolved during evolution of the metazoans to regulate growth and development in these multicellular organisms. However, recent research is adding strength to the original phenotypic observations described almost a decade ago which indicated that some parasitic protozoa may have evolved a cell death pathway analogous to the process described as apoptosis in metazoa. Here we explore the implications of a programmed cell death pathway in the African tsetse-transmitted trypanosomes.

A Cell Death Pathway Induced by Antibody-Mediated Cross-Linking of CD45 on Lymphocytes

2003 ◽  
Vol 23 (5-6) ◽  
pp. 421-440 ◽  
Author(s):  
Ann-Muriel Steff ◽  
Marylene Fortin ◽  
Fabianne Philippoussis ◽  
Sylvie Lesage ◽  
Chantal Arguin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cross Linking ◽  
Cell Death Pathway ◽  
A Cell

NETosis: how vital is it?

Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2784-2794 ◽  
Author(s):  
Bryan G. Yipp ◽  
Paul Kubes
Keyword(s):  
Innate Immunity ◽  
Cell Death ◽  
Critical Role ◽  
Neutrophil Extracellular Traps ◽  
Live Cell ◽  
Extracellular Traps ◽  
Cell Death Pathway ◽  
A Cell ◽  
Net Release

Abstract In this review, we examine the evidence that neutrophil extracellular traps (NETs) play a critical role in innate immunity. We summarize how NETs are formed in response to various stimuli and provide evidence that NETosis is not universally a cell death pathway. Here we describe at least 2 different mechanisms by which NETs are formed, including a suicide lytic NETosis and a live cell or vital NETosis. We also evaluate the evidence for NETs in catching and killing pathogens. Finally, we examine how infections are related to the development of autoimmune and vasculitic diseases through unintended but detrimental bystander damage resulting from NET release.

scholarly journals Oxeiptosis—a cell death pathway to mitigate damage caused by radicals

2018 ◽  
Vol 25 (7) ◽  
pp. 1191-1193 ◽  
Author(s):  
Pietro Scaturro ◽  
Andreas Pichlmair
Keyword(s):  
Cell Death ◽  
Cell Death Pathway ◽  
A Cell

scholarly journals A Single-Amino-Acid Substitution in Obg Activates a New Programmed Cell Death Pathway in Escherichia coli

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
Liselot Dewachter ◽  
Natalie Verstraeten ◽  
Daniel Monteyne ◽  
Cyrielle Ines Kint ◽  
Wim Versées ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Surface ◽  
Single Amino Acid ◽  
Altruistic Behavior ◽  
Membrane Blebbing ◽  
Cell Death Pathway ◽  
Higher Eukaryotes ◽  
Multicellular Organisms

ABSTRACT Programmed cell death (PCD) is an important hallmark of multicellular organisms. Cells self-destruct through a regulated series of events for the benefit of the organism as a whole. The existence of PCD in bacteria has long been controversial due to the widely held belief that only multicellular organisms would profit from this kind of altruistic behavior at the cellular level. However, over the past decade, compelling experimental evidence has established the existence of such pathways in bacteria. Here, we report that expression of a mutant isoform of the essential GTPase ObgE causes rapid loss of viability in Escherichia coli. The physiological changes that occur upon expression of this mutant protein—including loss of membrane potential, chromosome condensation and fragmentation, exposure of phosphatidylserine on the cell surface, and membrane blebbing—point to a PCD mechanism. Importantly, key regulators and executioners of known bacterial PCD pathways were shown not to influence this cell death program. Collectively, our results suggest that the cell death pathway described in this work constitutes a new mode of bacterial PCD. IMPORTANCE Programmed cell death (PCD) is a well-known phenomenon in higher eukaryotes. In these organisms, PCD is essential for embryonic development—for example, the disappearance of the interdigital web—and also functions in tissue homeostasis and elimination of pathogen-invaded cells. The existence of PCD mechanisms in unicellular organisms like bacteria, on the other hand, has only recently begun to be recognized. We here demonstrate the existence of a bacterial PCD pathway that induces characteristics that are strikingly reminiscent of eukaryotic apoptosis, such as fragmentation of DNA, exposure of phosphatidylserine on the cell surface, and membrane blebbing. Our results can provide more insight into the mechanism and evolution of PCD pathways in higher eukaryotes. More importantly, especially in the light of the looming antibiotic crisis, they may point to a bacterial Achilles’ heel and can inspire innovative ways of combating bacterial infections, directed at the targeted activation of PCD pathways.

New in vitro insights on a cell death pathway induced by magnolol and honokiol in aristolochic acid tubulotoxicity

2016 ◽  
Vol 87 ◽  
pp. 77-87 ◽  
Author(s):  
Valérian Bunel ◽  
Marie-Hélène Antoine ◽  
Caroline Stévigny ◽  
Joëlle Nortier ◽  
Pierre Duez
Keyword(s):  
Cell Death ◽  
Aristolochic Acid ◽  
Cell Death Pathway ◽  
A Cell

scholarly journals Effect of dietary flavonols on oestrogen receptor transactivation and cell death induction

2004 ◽  
Vol 91 (6) ◽  
pp. 831-839 ◽  
Author(s):  
Lai K. Leung ◽  
Lai See Po ◽  
Tak Yee Lau ◽  
Yee Man Yuen
Keyword(s):  
Cell Death ◽  
Hepg2 Cells ◽  
Oestrogen Receptor ◽  
Transcriptional Activity ◽  
Fruits And Vegetables ◽  
Free System ◽  
Plant Foods ◽  
Structural Resemblance ◽  
A Cell ◽  
Mcf 7

Consumption of fruits and vegetables has been associated with cancer prevention; flavonoids are widely distributed in plant foods and considered to be the active ingredients. Quercetin and kaempferol are two of the most commonly found dietary flavonols, and have been reported to prevent cancer. We have previously reported that the isoflavone genistein and the flavone baicalein exert differential actions on the oestrogen receptor (OR) α in HepG2 cells. Because of the structural resemblance to both isoflavone and flavone, we examined the effects of these dietary flavonols on ORα– and ORβ–specific transactivations and their subsequent involvement in inducing MCF-7 cell death. In the present study, both quercetin and kaempferol were able to compete for OR binding in a cell-free system and were agonistic to ORα and -β expressed in HepG2 cells, while some additive effect was observed in the oestrogen response element (ORE)-driven transcription when 17β-oestradiol was co-administered. Since the bcl-2 promoter contained two ORE, and ORE-driven transcriptional activity and Bcl-2 mRNA expression were increased by treatment with 10 μm-quercetin or kaempferol, it is possible that quercetin and kaempferol might up-regulate Bcl-2 expression through OR transactivation in MCF-7 cells. Cell death ELISA assay performed on MCF-7 cells indicated that an increase of apoptosis occurred at 25 μm-, but not 10 μm-, quercetin or kaempferol. Indirectly the results suggest that OR activation is not sufficient to induce apoptosis and that apoptosis is induced despite an increase in Bcl-2 expression.

scholarly journals Increased Nuclear Apoptosis-Inducing Factor after Transient Focal Ischemia: A 12/15-Lipoxygenase-dependent Organelle Damage Pathway

2010 ◽  
Vol 30 (6) ◽  
pp. 1157-1167 ◽  
Author(s):  
Stefanie Pallast ◽  
Ken Arai ◽  
Anton Pekcec ◽  
Kazim Yigitkanli ◽  
Zhanyang Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Glutathione Depletion ◽  
Established Cell Line ◽  
Edema Formation ◽  
Cell Death Pathway ◽  
Nuclear Apoptosis ◽  
Apoptosis Inducing Factor

12/15-lipoxygenase (12/15-LOX) contributes to acute neuronal injury and edema formation in mouse models of middle cerebral artery occlusion (MCAO). The apoptosis-inducing factor (AIF) is implicated in caspase-independent forms of apoptosis, and has been linked to ischemic neuronal cell death. We show here that increased AIF in the peri-ischemic cortex of mouse colocalizes with 12/15-LOX after 2 h of MCAO. The 12/15-LOX inhibitor baicalein prevents the increase and nuclear localization of AIF, suggesting this pathway may be partially responsible for the neuroprotective qualities of baicalein. Using an established cell line model of neuronal oxidative stress, we show that 12/15-LOX activated after glutathione depletion leads to AIF translocation to the nucleus, which is abrogated by the 12/15-LOX inhibitor baicalein (control: 19.3%±6.8% versus Glutamate: 64.0%±8.2% versus glutamate plus baicalein: 11.4%±2.2%). Concomitantly, resident proteins of the ER are dispersed throughout the cell (control: 31.0%±8.4% versus glutamate: 70.0%±5.5% versus glutamate plus baicalein: 8.0%±2.7%), suggesting cell death through organelle damage. Taken together, these findings show that 12/15-LOX and AIF are sequential actors in a common cell death pathway that may contribute to stroke-induced brain damage.

scholarly journals Role of the Crosstalk between Autophagy and Apoptosis in Cancer

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Minfei Su ◽  
Yang Mei ◽  
Sangita Sinha
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Cancer Therapeutics ◽  
Coordinate Regulation ◽  
Macromolecular Assemblies ◽  
Cell Death Pathway ◽  
Survival Pathway ◽  
A Cell ◽  
Type Ii Cell

Autophagy and apoptosis are catabolic pathways essential for organismal homeostasis. Autophagy is normally a cell-survival pathway involving the degradation and recycling of obsolete, damaged, or harmful macromolecular assemblies; however, excess autophagy has been implicated in type II cell death. Apoptosis is the canonical programmed cell death pathway. Autophagy and apoptosis have now been shown to be interconnected by several molecular nodes of crosstalk, enabling the coordinate regulation of degradation by these pathways. Normally, autophagy and apoptosis are both tumor suppressor pathways. Autophagy fulfils this role as it facilitates the degradation of oncogenic molecules, preventing development of cancers, while apoptosis prevents the survival of cancer cells. Consequently, defective or inadequate levels of either autophagy or apoptosis can lead to cancer. However, autophagy appears to have a dual role in cancer, as it has now been shown that autophagy also facilitates the survival of tumor cells in stress conditions such as hypoxic or low-nutrition environments. Here we review the multiple molecular mechanisms of coordination of autophagy and apoptosis and the role of the proteins involved in this crosstalk in cancer. A comprehensive understanding of the interconnectivity of autophagy and apoptosis is essential for the development of effective cancer therapeutics.

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