Journal Article•
Classification of Cell Death
01 Oct 2013-Journal of entomology and zoology studies (AkiNik Publications)-Vol. 1, Iss: 5, pp 120-126
TL;DR: Although cell death is known as apoptosis ve necrosis, molecular studies add to morphological studies and according to this, this classification is extended and there are diffirent types of cell death in terms of signal pathway.
Abstract: In 1972 Kerr and colleagues collect the cell death under two headings. Although cell death is known as apoptosis ve necrosis, molecular studies add to morphological studies and according to this, this classification is extended. In 2009 NCCD classifies it entosis, mitotic collapse, necrosis, necropitosis and pyroptosis by using terminological words. In addition to these there are diffirent types of cell death in terms of signal pathway. These are autophagic cell death, carnification cell death, netoz cell death, partanatoz cell death, anoikis cell death. In this article these types of cell death is noticed in detail.
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University of California, Davis1, Virginia Tech2, University of North Carolina at Chapel Hill3, University of Birmingham4, University of Manchester5, Kyoto University6, Saitama University7, Rutgers University8, University of Copenhagen9, Aberystwyth University10, Durham University11, James Hutton Institute12, Ghent University13, Oregon State University14, Wageningen University and Research Centre15, Karolinska Institutet16, Swedish University of Agricultural Sciences17
TL;DR: A classification based on morphological criteria is suggested of PCD associated with the hypersensitive response to biotrophic pathogens, which can express features of both necrosis and vacuolar cell death, PCD in starchy cereal endosperm and during self-incompatibility.
Abstract: Programmed cell death (PCD) is an integral part of plant development and of responses to abiotic stress or pathogens. Although the morphology of plant PCD is, in some cases, well characterised and molecular mechanisms controlling plant PCD are beginning to emerge, there is still confusion about the classification of PCD in plants. Here we suggest a classification based on morphological criteria. According to this classification, the use of the term 'apoptosis' is not justified in plants, but at least two classes of PCD can be distinguished: vacuolar cell death and necrosis. During vacuolar cell death, the cell contents are removed by a combination of autophagy-like process and release of hydrolases from collapsed lytic vacuoles. Necrosis is characterised by early rupture of the plasma membrane, shrinkage of the protoplast and absence of vacuolar cell death features. Vacuolar cell death is common during tissue and organ formation and elimination, whereas necrosis is typically found under abiotic stress. Some examples of plant PCD cannot be ascribed to either major class and are therefore classified as separate modalities. These are PCD associated with the hypersensitive response to biotrophic pathogens, which can express features of both necrosis and vacuolar cell death, PCD in starchy cereal endosperm and during self-incompatibility. The present classification is not static, but will be subject to further revision, especially when specific biochemical pathways are better defined.
502 citations
Cites background or methods from "Classification of Cell Death"
...is often associated with activation of caspases and oligonucleosomal fragmentation of DNA, these processes can also take place during non-apoptotic cell death, and are thus insufficient criteria for assignment.(1)...
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...Lysosomal events include ROS production and permeabilisation of the lysosomal membrane causing release of active cathepsin proteases to the cytosol.(1,31)...
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...various organelles, early rupture of the plasma membrane and loss of intracellular content.(1,30) Although it is no longer considered to be an unprogrammed process, necrosis...
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...ways, it is possible to begin classifying plant cell death scenarios based on morphological criteria, as was initially the case in animal cell death research(2,3) and is still used for the classification of cell death in animal science.(1) This document attempts to provide a classification of plant cell death....
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...and necrosis – apoptosis is much better understood, both cytologically and biochemically.(1,4) Apoptosis is accompanied by rounding up of the cell, reduction of cellular volume, chromatin...
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Journal Article•
TL;DR: In this paper, the authors describe a non-apoptotic cell death program in matrix-detached cells, termed entosis, that is initiated by a previously unrecognized and unusual process involving the invasion of one cell into another, leading to a transient state in which a live cell is contained within a neighboring host cell.
Abstract: 1560 Epithelial cells require attachment to extra-cellular matrix (ECM) to suppress an apoptotic cell death program termed anoikis. We describe a non-apoptotic cell death program in matrix-detached cells, termed entosis, that is initiated by a previously unrecognized and unusual process involving the invasion of one cell into another, leading to a transient state in which a live cell is contained within a neighboring host cell. These 9cell-in-cell9 structures closely resemble similar cytological features in human cancers. Although a small percentage of live internalized cells can be released, the majority of internalized cells undergo non-apoptotic cell death by lysosomal acidification. Based on these data, we present evidence for a tumor suppressive role of entosis in human breast cancer. Paradoxically, we have also found that entosis can promote the development of aneuploidy, as live internalized cells can disrupt cytokinesis of host cells leading to multinucleation in vitro and in vivo. Thus, entosis may be tumor suppressive in some contexts and paradoxically tumor promoting in others. Models to investigate the role of entosis in human tumors will be presented.
446 citations
TL;DR: Understanding the underlying molecular mechanism of lipid metabolism and the function of different lipid molecules could provide the basis for cancer cell death rationale, discover novel and potential targets, and develop new anticancer drugs for cancer therapy.
Abstract: Lipid metabolism is regulated by multiple signaling pathways, and generates a variety of bioactive lipid molecules. These bioactive lipid molecules known as signaling molecules, such as fatty acid, eicosanoids, diacylglycerol, phosphatidic acid, lysophophatidic acid, ceramide, sphingosine, sphingosine-1-phosphate, phosphatidylinositol-3 phosphate, and cholesterol, are involved in the activation or regulation of different signaling pathways. Lipid metabolism participates in the regulation of many cellular processes such as cell growth, proliferation, differentiation, survival, apoptosis, inflammation, motility, membrane homeostasis, chemotherapy response, and drug resistance. Bioactive lipid molecules promote apoptosis via the intrinsic pathway by modulating mitochondrial membrane permeability and activating different enzymes including caspases. In this review, we discuss recent data in the fields of lipid metabolism, lipid-mediated apoptosis, and cancer therapy. In conclusion, understanding the underlying molecular mechanism of lipid metabolism and the function of different lipid molecules could provide the basis for cancer cell death rationale, discover novel and potential targets, and develop new anticancer drugs for cancer therapy.
307 citations
Cites background from "Classification of Cell Death"
...Three types of cell death can be distinguished in mammalian cells according to morphological criteria: autophagy, necrosis and apoptosis [89]....
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TL;DR: This work discusses current combinatorial approaches to convert otherwise non-immunogenic instances of RCD into bona fide ICD, and suggests that novel therapeutic regimens that trigger ICD are urgently awaited.
Abstract: The term “immunogenic cell death” (ICD) is commonly employed to indicate a peculiar instance of regulated cell death (RCD) that engages the adaptive arm of the immune system. The inoculation of cancer cells undergoing ICD into immunocompetent animals elicits a specific immune response associated with the establishment of immunological memory. Only a few agents are intrinsically endowed with the ability to trigger ICD. These include a few chemotherapeutics that are routinely employed in the clinic, like doxorubicin, mitoxantrone, oxaliplatin, and cyclophosphamide, as well as some agents that have not yet been approved for use in humans. Accumulating clinical data indicate that the activation of adaptive immune responses against dying cancer cells is associated with improved disease outcome in patients affected by various neoplasms. Thus, novel therapeutic regimens that trigger ICD are urgently awaited. Here, we discuss current combinatorial approaches to convert otherwise non-immunogenic instances of RCD into bona fide ICD.
305 citations
TL;DR: The most recent discoveries in apoptosis regulation and possible mechanisms for resensitizing tumor cells to therapy are reviewed.
Abstract: The process of apoptosis is essential for maintaining the physiologic balance between cell death and cell growth. This complex process is executed by two major pathways that participate in activating an executioner mechanism leading to chromatin disintegration and nuclear fragmentation. Dysregulation of these pathways often contributes to cancer development and resistance to cancer therapy. Here, we review the most recent discoveries in apoptosis regulation and possible mechanisms for resensitizing tumor cells to therapy.
231 citations
References
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TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
Abstract: The term apoptosis is proposed for a hitherto little recognized mechanism of controlled cell deletion, which appears to play a complementary but opposite role to mitosis in the regulation of animal cell populations. Its morphological features suggest that it is an active, inherently programmed phenomenon, and it has been shown that it can be initiated or inhibited by a variety of environmental stimuli, both physiological and pathological.The structural changes take place in two discrete stages. The first comprises nuclear and cytoplasmic condensation and breaking up of the cell into a number of membrane-bound, ultrastructurally well-preserved fragments. In the second stage these apoptotic bodies are shed from epithelial-lined surfaces or are taken up by other cells, where they undergo a series of changes resembling in vitro autolysis within phagosomes, and are rapidly degraded by lysosomal enzymes derived from the ingesting cells.Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development. It occurs spontaneously in untreated malignant neoplasms, and participates in at least some types of therapeutically induced tumour regression. It is implicated in both physiological involution and atrophy of various tissues and organs. It can also be triggered by noxious agents, both in the embryo and adult animal.
15,416 citations
"Classification of Cell Death" refers background in this paper
...These are Apoptosis (programed cell death which is controled as genetic) and necrosis (accidental and unprogrammed cell death) [1]....
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University of Paris-Sud1, Institut Gustave Roussy2, French Institute of Health and Medical Research3, Ghent University4, University of Texas Southwestern Medical Center5, Thomas Jefferson University6, University of Massachusetts Medical School7, University of Pennsylvania8, Centre national de la recherche scientifique9, University of Zurich10, University College London11, Discovery Institute12, University of California, San Diego13, Salk Institute for Biological Studies14, Istituto Superiore di Sanità15, University of Michigan16, University of Chicago17, University of Lausanne18, Harvard University19, University of Rome Tor Vergata20, Karolinska Institutet21, University of Leicester22
TL;DR: This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including ‘entosis’, ‘mitotic catastrophe”,’ ‘necrosis‚ ‘necroptosis‚’ and ‘pyroptotic’.
Abstract: Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like 'percentage apoptosis' and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that 'autophagic cell death' is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including 'entosis', 'mitotic catastrophe', 'necrosis', 'necroptosis' and 'pyroptosis'.
3,005 citations
"Classification of Cell Death" refers background in this paper
...Classification of cell death: According to Kroemer and collegues [3] cell death is classified under four types....
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TL;DR: It is demonstrated that necroptosis contributes to delayed mouse ischemic brain injury in vivo through a mechanism distinct from that of apoptosis and offers a new therapeutic target for stroke with an extended window for neuroprotection.
Abstract: The mechanism of apoptosis has been extensively characterized over the past decade, but little is known about alternative forms of regulated cell death. Although stimulation of the Fas/TNFR receptor family triggers a canonical 'extrinsic' apoptosis pathway, we demonstrated that in the absence of intracellular apoptotic signaling it is capable of activating a common nonapoptotic death pathway, which we term necroptosis. We showed that necroptosis is characterized by necrotic cell death morphology and activation of autophagy. We identified a specific and potent small-molecule inhibitor of necroptosis, necrostatin-1, which blocks a critical step in necroptosis. We demonstrated that necroptosis contributes to delayed mouse ischemic brain injury in vivo through a mechanism distinct from that of apoptosis and offers a new therapeutic target for stroke with an extended window for neuroprotection. Our study identifies a previously undescribed basic cell-death pathway with potentially broad relevance to human pathologies.
2,397 citations
"Classification of Cell Death" refers background in this paper
...Morphological characterization is that increasing in the volume of cell, swelling of organelles, plasma membrane rupture, followed by leakage of intracellular contents [27]....
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TL;DR: It is shown that PARP-1 activation is required for translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus and that AIF is necessary for PARp-1–dependent cell death.
Abstract: Poly(ADP-ribose) polymerase-1 (PARP-1) protects the genome by functioning in the DNA damage surveillance network. PARP-1 is also a mediator of cell death after ischemia-reperfusion injury, glutamate excitotoxicity, and various inflammatory processes. We show that PARP-1 activation is required for translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus and that AIF is necessary for PARP-1–dependent cell death. N -methyl- N ′-nitro- N -nitrosoguanidine, H2O2, and N -methyl-d-aspartate induce AIF translocation and cell death, which is prevented by PARP inhibitors or genetic knockout of PARP-1, but is caspase independent. Microinjection of an antibody to AIF protects against PARP-1–dependent cytotoxicity. These data support a model in which PARP-1 activation signals AIF release from mitochondria, resulting in a caspase-independent pathway of programmed cell death.
1,781 citations
TL;DR: F Fas kills activated primary T cells efficiently in the absence of active caspases, which results in necrotic morphological changes and late mitochondrial damage but no cytochrome c release.
Abstract: Cell death is achieved by two fundamentally different mechanisms: apoptosis and necrosis. Apoptosis is dependent on caspase activation, whereas the caspase-independent necrotic signaling pathway remains largely uncharacterized. We show here that Fas kills activated primary T cells efficiently in the absence of active caspases, which results in necrotic morphological changes and late mitochondrial damage but no cytochrome c release. This Fas ligand-induced caspase-independent death is absent in T cells that are deficient in either Fas-associated death domain (FADD) or receptor-interacting protein (RIP). RIP is also required for necrotic death induced by tumor necrosis factor (TNF) and TNF-related apoptosis-inducing ligand (TRAIL). In contrast to its role in nuclear factor kappa B activation, RIP requires its own kinase activity for death signaling. Thus, Fas, TRAIL and TNF receptors can initiate cell death by two alternative pathways, one relying on caspase-8 and the other dependent on the kinase RIP.
1,734 citations
"Classification of Cell Death" refers background in this paper
...In this pathway activity of cool / treonin kinase is important but it is not needed for NF-κB activaiton and apoptosis [28]....
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