Apoptosis
Apoptosis is a programmed cell death process that occurs in multicellular organisms. It plays a crucial role in maintaining tissue homeostasis by eliminating unwanted or damaged cells. Apoptosis is characterized by distinct morphological and biochemical changes in the cell, ultimately leading to its controlled self-destruction.
7 Key excerpts on "Apoptosis"
eBook - ePub- Mohamed Al-Rubeai, A Nichol Emery, Mohamed Al-Rubeai, A Nichol Emery(Authors)
- 2020(Publication Date)
- CRC Press(Publisher)
...11 Analysis of Apoptosis by Flow Cytometry A NNE E. M ILNER, H ONG W ANG, AND C HRISTOPHER D. G REGORY The University of Birmingham, Birmingham, England I. INTRODUCTION A. Apoptosis: Physiological Cell Death The term Apoptosis describes a series of gross cellular changes characteristic of an active or programmed form of cell death that is now accepted as a physiological, as opposed to accidental, mode of cell deletion. Active cell death represents a normal control mechanism as profoundly important to multicellular organisms as cell proliferation or differentiation. In mammals, the significance of physiological cell death is illustrated by the removal of cells through activation of their apoptotic mechanism during tissue modeling and organogenesis in embryonic development, and in the control of homeostasis in a diversity of tissue types [1]. There is much evidence to support the view that programmed cell death is a cell-autonomous process [2]. It has also been suggested that, with few exceptions, all cells from all lineages are programmed to undergo active self-destruction unless they receive survival signals to suppress that program [3]. Apoptosis is a genetically regulated, thermodynamically demanding process that contrasts markedly with the passive mode of cell death, necrosis. Necrotic cells play no active role in their own demise, and the loss in membrane integrity that occurs during necrosis leads to leakage of intracellular contents and subsequent histotoxic damage and inflammation. In vivo, the process of Apoptosis is such that membrane integrity is retained until the dying cells have been cleared by phagocytosis...
- Gerhard Krauss(Author)
- 2014(Publication Date)
- Wiley-VCH(Publisher)
...17 Apoptosis Eukaryotic cells can self-destruct in an orderly, highly controlled process known as Apoptosis. The term Apoptosis, which was first coined following investigations of the nematode Caenorhabditis elegans, is of Greek origin and describes the “falling of leaves.” Activation of the apoptotic program involves the coordinated demolition of intracellular structures by members of the caspase family of proteases. This is accompanied by characteristic changes in cell morphology, such as condensation of the chromatin, the degradation of DNA, cell shrinkage, fragmentation of the cell nucleus, and disassembly into membrane-enclosed apoptotic vesicles. Apoptosis is based on a genetic program that forms an indispensable part of the development and function of an organism, and serves to eliminate any undesired or superfluous cells in a targeted manner. The functions of Apoptosis target the major biological processes of the cell, including: tissue homeostasis; the elimination of cells during differentiation and development; the elimination of cells during immune responses; and the elimination of damaged cells to avoid propagation of mutations and degeneration into tumor cells. The major part of the apoptotic program, which exists in the cell in a latent, inactive form, requires only an apoptotic stimulus to activate the program and to induce Apoptosis. Thus, apoptotic processes may be initiated within a short timescale, without the activation of transcription. Some forms of Apoptosis are also known that are dependent on transcription. Due to the potential deleterious consequences of an inappropriate activation of Apoptosis in normal cells, the apoptotic program is strictly controlled by the balanced input of pro-apoptotic and anti-apoptotic signals originating from internal and external sources. Many signals that feed into the apoptotic program are transmitted via cellular signaling pathways involved in the control of cell proliferation and homeostasis...
eBook - ePubThe Avian Erythrocyte
Its Phylogenetic Odyssey
- Chester A. Glomski, Alessandra Pica(Authors)
- 2016(Publication Date)
- CRC Press(Publisher)
...33 Apoptosis An interesting distinction regarding avian (chicken) erythrocytes as opposed to other cells relative to the maintenance of the cell’s viability has been recently brought to light. This feature is in regard to the mechanisms that induce or participate in the self-directed demise of the erythrocyte (i.e., cell death). This form of selected cell elimination from an identified group of an organism’s cells has been termed Apoptosis. Apoptosis or programmed cell death is a form of cell suicide that permits an organism to efficiently remove its redundant, abnormal, or aged cells. This process is conducted for the benefit of the organism and is executed without affecting the remaining desired cells. The key biochemical component of this phenomenon is a family of aspartic acid-directed cysteine proteases called caspases. These cysteine-dependent aspartate proteases have the capability of cleaving many vital cell substrates thereby leading to the cell’s demise. The true caspases are restricted to the metazoans. Four caspase-like proteins have been identified in the well recognized, tiny, 1mm-long, soil-living nematode (roundworm) Caenorhabditis elegans while seven have been found in the fruit fly Drosophila, and about 15 have been identified in mammals. Apoptosis genes have been described, in the zebra fish Danio rerio and in the Atlantic salmon Salmo salar. A definite increase in the number and complexity of the apoptotic protein components has evolved up through the mammals. It has been concluded that there has been a remarkable conservation of Apoptosis pathways between fish and mammals. Caspase-dependent Apoptosis has been shown to have multiple pathways. In one so-called extrinsic pathway signaling agents bind to cell surface receptors while an intrinsic pathway is activated by signals arising within the cell. In the latter instance one of mechanisms is targeting the functionality of the mitochondria...
eBook - ePub- Ronni Wolf, Lawrence Charles Parish, Jennifer L. Parish, Ronni Wolf, Lawrence Charles Parish, Jennifer L. Parish(Authors)
- 2017(Publication Date)
- CRC Press(Publisher)
...We emphasize the apoptotic pathway, considered for years the hallmark of PCD, and the different stimuli that produce cell injury. CELL INJURY The survival of multicellular organisms depends on the function of a diverse set of differentiated cell types. After development is complete, the viability of the organism depends on the maintenance and renewal of these diverse lineages. Within each lineage homeostasis is maintained through a delicate balance between cell proliferation and cell death. 1 Disorders of either process have pathologic consequences and can lead to disturbed embryogenesis, neurodegenerative diseases, or the development of cancer 2 ; therefore, the equilibrium between life and death is tightly controlled, and faulty elements can effectively be eliminated by PCD, a term that well defines the planned sequence of physiological cellular autodestruction, which requires both energy expenditure and a specific enzymatic network. Cell death is an essential strategy for the control of the dynamic balance of the living system, and it is the ultimate result of most physiological as well as pathological processes. Skulachev aptly described the concept of cell death using the metaphor of the “Samurai law of biology” (i.e., it is better to die than be wrong), showing that the suicide program is a way to purify cells of damaged organelles and tissues of unwanted cells that use up valuable substrates and nutrients. 3, 4 Cell death thus appears as the unique solution to eliminate what is unwanted or dangerous to the “community.” 3, 5 In the past, PCD was mainly associated with Apoptosis, a death process characterized by morphologic changes such as shrinkage of the cell, condensation of chromatin, and disintegration of the cell into small fragments (so-called “apoptotic bodies”) that are removed by phagocytosis...
eBook - ePub- Matthew Dickinson, James Beynon, Matthew Dickinson, James Beynon(Authors)
- 2020(Publication Date)
- CRC Press(Publisher)
...Initially, the definition was confined to a clear sequence of morphological events that characterise this PCD (Kerr et al., 1972; see also section 7.2). More recently, however, key proteins that execute cell death, cysteine proteases termed caspases, and the complex mitochondrion-based machinery that regulates them, have become synonymous with Apoptosis (see section 7.3). Nevertheless, in both yeast and animals, apoptotic cell death morphology has been described in the absence of caspases (see section 7.4), suggesting that the morphology of cell death is more important to the definition of Apoptosis, and also that there is more than one pathway to its execution. With this in mind, this chapter aims to describe the pathogen-induced HR in plants and to discuss whether it should be called Apoptosis. 7.2 Comparison of the morphologies of Apoptosis in animals and PCD in the plant hypersensitive response Apoptosis is characterised by a distinct set of morphological features (Kerr et al., 1972). Initially, both chromatin and cytoplasm condense and nuclear and cellular outlines appear convoluted or lobed. The cells are seen to shrink. Shortly after this, the nucleus disintegrates and DNA fragmentation occurs. The cells then fragment to form membrane-bound apoptotic bodies containing intact organelles. Apoptotic bodies are finally phagocytosed by neighbouring cells or macrophages. While there are several signalling routes leading to Apoptosis (see section 7.3), chromatin condensation and nuclear DNA fragmentation are common features of the process. A number of cytometric techniques have been central to studying these events. Chromatin condensation may be detected by staining nuclei with propidium iodide (PI) and measuring the level of fluorescence. During Apoptosis, there is a reduction in fluorescence due to less PI intercalatory binding as DNA coiling tightens (Darzynkiewicz et al., 1992)...
eBook - ePub- John E. Niederhuber, James O. Armitage, James H Doroshow, Michael B. Kastan, Joel E. Tepper(Authors)
- 2019(Publication Date)
- Elsevier(Publisher)
...5.1). 51 Necrosis Classically, necrosis was defined as an instance of cell death lacking the peculiar morphological manifestations of Apoptosis as well as the accumulation of cytoplasmic vacuoles that characterize autophagic cells. Somehow, this was in line with the belief that necrosis would always proceed in an unregulated fashion and would only terminate accidental instances of cell death. 5 In the 1990s, Vandenabeele's and Schulze-Osthoff's groups demonstrated that engagement of FAS does not always lead to cell death via extrinsic Apoptosis. 52 – 54 This observation instilled in some researchers the suspicion that, similar to Apoptosis, necrosis also might be orchestrated by a refined molecular machinery; this ignited an intense wave of research that has not yet come to an end. 6 Important to note, regulated necrosis occurs during mammalian development, in particular at the bone growth plate (i.e., the zone of the bone that controls its length), as well as during adult tissue homeostasis, for instance in the lower regions of intestinal crypts. 55, 56 Moreover, multiple instances of necrotic RCD have been involved in the pathophysiology of diseases including viral infection, neurodegeneration, ischemia, and others. 8, 22, 57 Necroptosis The best-characterized pathway of regulated necrosis, which is known as necroptosis, can be elicited by the ligation of death receptors in conditions in which CASP8 is inhibited (either by pharmacologic or by genetic interventions)...
eBook - ePub- Richard A Lockshin, Zahra Zakeri(Authors)
- 2015(Publication Date)
- Richard A Lockshin(Publisher)
...Chapter 14: Discovery of key mechanisms of cell death: from Apoptosis to necroptosis (Yuan) Junying Yuan. Department of Cell Biology, Harvard Medical School, 240 Longwood Ave. Boston, MA 02115. USA Abstract: This essay provides a brief account of my 30+ years of research in the field of cell death that has, thus far, led to the discovery of caspases in regulating Apoptosis in mammals and a form of regulated necrosis known as necroptosis. My discoveries have demonstrated the molecular mechanisms of regulated cell death in mammalian cells, refuted the dogma that claimed necrosis to only be a passive form of cell death, and introduced the possibility of targeting necrosis in the treatment of human diseases. Introduction My interest in cell death was inspired by the specific loss of neuronal cells during normal embryonic development and during neurodegeneration that I had learned in the classes as a first-year graduate student at the Harvard Medical School in early 1980’s. This interest compelled me to join the laboratory of Dr. H. R. Horvitz at MIT, where I studied mechanisms of programmed cell death in the nematode C. elegans as a part of my Ph.D. research. After obtaining my Ph.D. in Neurosciences from Harvard in 1989, I went on to establish my own laboratory at the Cardiovascular Research Center at Massachusetts General Hospital, intending to investigate the idea that mammalian cells might possess a genetically encoded, programmed cell death mechanism similar to what I had found in the nematode C. elegans...
