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Dead cell, according to Nomenclature Committee on Cell Death (NCCD), is the cell that displays any one of the properties that are listed below:

  • Disappearance of plasma membrane integrity, in vivo.
  • Complete fragmentation of nucleus and other components of cell into separate partition.
  • Engulfment of these partitions by adjacent cell, in vivo [1].

Two major classes of cell death in terms of their functional aspects named Programmed and non-Programmed cell death [2]. While programmed cell death (PCD) occurs in an organized manner via intracellular processes, non- PCD, attributed to necrosis, has unorganized style. Non- PCD generally sourced from acute injury and infection. In general, PCD is observed in biological development operations, cancer therapies and cancer propagation[3].

Figure 1. Types of cell death and their aspects

Apoptosis

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Apoptosis is one of the type of cell death which have signal transduction path as seen in Figure 2.

Figure 2. Illustration describes signal transduction pathway of apoptosis.

As last step of apoptosis cell is divided to minor parts named apoptotic bodies. These bodies are cleared by phagocytes and then processed via the help of lysosomal enzymes. By this way, release of particles that may cause inflammation is prevented [4].

Autophagy

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Autophagy provides degradation by the help of autophagic vacuoles [5]. The process start with collection of cytoplasmic elements into autophagosomes, a double membraned compartment. After that these compartments combine with lysosome. Via this event degradation of collected materials is aimed and achieved [6] Cell exposing to autophagy can be processed by neighboring cells, by phagocytosis[7][8].

Programmed Necrosis

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Apoptosis and autophagy were known as sole styles of PCD before programmed necrosis emerges. Programmed necrosis includes subtypes, necroptosis, pyroptosis, partonatos and ferroptosis [9]. These newly discovered subtypes may provide solution for cancers that has ability to escape from apoptosis [10]. Among four subtypes of programmed necrosis, necroptosis is the best described one [11].

Necroptosis

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Prevalenly, induction of necroptosis takes place by the help trigger of death receptor. Because this type of PCD shares similarities with both necrosis and apoptosis, necroptosis name is given as a combination of names necrosis and apoptosis. Necroptosis utilizes organized cellular particles, as seen in apoptosis, while result in burst of cell, like diagnosed in necrosis. Burst of the cell causes release of damage- associated molecular patterns (DAMPs)[12].

Figure 3. Emergence of the name necroptosis.

Parthonatos

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Parthonatos is the cell that is triggered via overstimulation of PARP. PARP is a DNA repairing enzyme which means it can be activated by providing genotoxic- stress [13].

Pyroptosis

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Pyroptosis uses inflammatory caspases, this condititon makes it highly inflammatory. Pathological agent, cancer and other some physiological issues result in pyroptosis. Initiation of the cell death begins with emergence of active multi- protein coımplex inflammasomes. Presence of Gasdermin D, found in the structure of inflammasomes and behaves as a substrate for inflammatory aspases, is an obligation for pyrotosis [14][15]. • Pro-inflammatory programmed cell death different than apoptosis -Involves activation of caspase-1 which cleaves the precursor form of IL-1 to generate biologically active IL-1 (fever inducing cytokine). • Important in the host defense system for fighting microbial pathogens – In monocytes, macrophages, and dendritic cells infected with certain microbes – Microbial pathogens that may be killed by pyroptosis 

  -Salmonella typhimurium, Shigella flexneri, Legionella pneumophila, Pseudomonas aeruginosa, Candida albicans, Adenovirus, and Influenza virus

• Also implicated in pathogenesis of – Myocardial infarction (MI), Neurodegenerative diseases, Inflammatory Bowel Disease (IBD), Cerebral Ischemia, and Endotoxic Shock.

Ferroptosis

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Ferroptosis observed in various degenerative diseases. The reason that drives cell to ferroptosis is accumulation lethal ROS in an intracellular iron- dependent manner. Ferroptosis is fairly related with peroxidation of lipids. Lowered level of functioning of glutathione preoxidase 4 (GPX4), a lipid repair enzyme and it is able to prevent ferroptosis, and accumulation of lipid preoxidase provoke ferroptosis. Disrupted outer membrane of mitochondria, increased mitochondrial membrane density and decrease in the overall size of the mitochondria are the signs of ferroptosis[16][17].

Cell death in plants

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In plants apoptotic bodies cannot found because of presence of cell wall. And another difference in plant cell death is lack of phagocytes in plants. Therefore, it is not true to catagorize death of a plant cell as apoptosis, even regardless of the aspects[18].

Lytic vacuoles take care of recycling of cell components, as lysosome do this job in animal cells[19]. These vacuoles play an significant role at a special type of a cell death called vacuolar cell death[20]. Vacuolar cell death functions via sliding of cytoplasmic content to lytic vacuole and fallowed by dismantlement of slided cytoplasmic elements [21]. Mitochondria and other organels remain intact till vacuole membrane is disrupted. While in some cases, high degree degradation of cell wall occurs, as seen in aerenchyma formation, it is not observed in other cases like differentiation of xylem cells of vascuolar plants[22][23][24].

Some aspects of vacuolar cell death:

  • Big lytic vacuoles are generated.
  • Nuclear envelope disrupted.
  • Vacuolar membrane (tonoplast) is ruptured.

Some aspects of necrosis in plant cells:

  • Mitochondria gain water from cytoplasm so it is swelling.
  • Plasma membrane is disrupted in early phase of the death process.
  • Cell corpse remains mostly unprocessed (because plants are devoid of phagocyte cells).
  • Protoplast shrinks however no visual alteration is able to seen at overall structure of the plant cell.

Hyper sensitive response displays aspects that are combination of vacuolar cell death and necrosis[25].

References

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  1. ↑ Kroemer, G., et al. (2009). "Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009." Cell death and differentiation 16(1): 3.
  2. ↑ Melino G. The Sirens’ song. Nature 2001;412:23.
  3. ↑ Jouan-Lanhouet, S., et al. (2014). Necroptosis, in vivo detection in experimental disease models. Seminars in Cell & Developmental Biology, Elsevier.
  4. ↑ Kroemer, G., et al. (2009). "Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009." Cell death and differentiation 16(1): 3.
  5. ↑ Clarke, P. G. (1990). "Developmental cell death: morphological diversity and multiple mechanisms." Anatomy and embryology 181(3): 195-213.
  6. ↑ Klionsky, D. J. and S. D. Emr (2000). "Autophagy as a regulated pathway of cellular degradation." Science 290(5497): 1717-1721.
  7. ↑ Clarke, P. G. (1990). "Developmental cell death: morphological diversity and multiple mechanisms." Anatomy and embryology 181(3): 195-213.
  8. ↑ Schweichel, J. U. and H. J. Merker (1973). "The morphology of various types of cell death in prenatal tissues." Teratology 7(3): 253-266.
  9. ↑ Jouan-Lanhouet, S., et al. (2014). Necroptosis, in vivo detection in experimental disease models. Seminars in Cell & Developmental Biology, Elsevier.
  10. ↑ Kim, B. (2017). "The Implications of Several Forms of Programmed Necrosis for Cancer Therapy." J Cancer Sci Ther 9: 630-635.
  11. ↑ Belizário, J., et al. (2015). "Necroptotic cell death signaling and execution pathway: lessons from knockout mice." Mediators of inflammation 2015.
  12. ↑ Degterev, A., et al. (2005). "Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury." Nature chemical biology 1(2): 112.
  13. ↑ Yu, S.-W., et al. (2002). "Mediation of poly (ADP-ribose) polymerase-1-dependent cell death by apoptosis-inducing factor." Science 297(5579): 259-263.
  14. ↑ He, W.-t., et al. (2015). "Gasdermin D is an executor of pyroptosis and required for interleukin-1β secretion." Cell research 25(12): 1285.
  15. ↑ Shi, J., et al. (2017). "Pyroptosis: gasdermin-mediated programmed necrotic cell death." Trends in biochemical sciences 42(4): 245-254.
  16. ↑ Angeli, J. P. F., et al. (2014). "Inactivation of the ferroptosis regulator Gpx4 triggers acute renal failure in mice." Nature cell biology 16(12): 1180.
  17. ↑ Yang, W. S., et al. (2014). "Regulation of ferroptotic cancer cell death by GPX4." Cell 156(1-2): 317-331.
  18. ↑ Van Doorn, W., et al. (2011). "Morphological classification of plant cell deaths." Cell death and differentiation 18(8): 1241.
  19. ↑ Müntz, K. (2007). "Protein dynamics and proteolysis in plant vacuoles." Journal of experimental botany 58(10): 2391-2407.
  20. ↑ Fath, A., et al. (2001). "Enzymes that scavenge reactive oxygen species are down-regulated prior to gibberellic acid-induced programmed cell death in barley aleurone." Plant physiology 126(1): 156-166.
  21. ↑ Van Doorn, W., et al. (2011). "Morphological classification of plant cell deaths." Cell death and differentiation 18(8): 1241.
  22. ↑ Drew, M. C., et al. (2000). "Programmed cell death and aerenchyma formation in roots." Trends in plant science 5(3): 123-127.
  23. ↑ Gunawardena, A. H. (2007). "Programmed cell death and tissue remodelling in plants." Journal of experimental botany 59(3): 445-451.
  24. ↑ Courtois‐Moreau, C. L., et al. (2009). "A unique program for cell death in xylem fibers of Populus stem." The Plant Journal 58(2): 260-274.
  25. ↑ Van Doorn, W., et al. (2011). "Morphological classification of plant cell deaths." Cell death and differentiation 18(8): 1241.
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