scholarly journals Anastasis: recovery from the brink of cell death

2018 ◽  
Vol 5 (9) ◽  
pp. 180442 ◽  
Author(s):  
Ho Man Tang ◽  
Ho Lam Tang
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cultured Cells ◽  
Mechanisms Of Action ◽  
Cell Recovery ◽  
Therapeutic Implications ◽  
Dying Cells ◽  
Late Stages ◽  
New Strategies ◽  
Natural Cell

Anastasis is a natural cell recovery phenomenon that rescues cells from the brink of death. Programmed cell death such as apoptosis has been traditionally assumed to be an intrinsically irreversible cascade that commits cells to a rapid and massive demolition. Interestingly, recent studies have demonstrated recovery of dying cells even at the late stages generally considered immutable. Here, we examine the evidence for anastasis in cultured cells and in animals, review findings illuminating the potential mechanisms of action, discuss the challenges of studying anastasis and explore new strategies to uncover the function and regulation of anastasis, the identification of which has wide-ranging physiological, pathological and therapeutic implications.

scholarly journals Anastasis: Cell Survival Mechanism

2020 ◽  
Vol 6 (1) ◽  
pp. 5-11
Author(s):  
Abolaji S. Olagunju ◽  
◽  
Folashade G. Olorunfemi ◽  
John O. Teibo ◽  
Abiodun M. Adewolu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Normal Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cell Recovery ◽  
Mesenchymal Transition ◽  
Rapid Destruction ◽  
Dying Cells ◽  
Late Stages ◽  
Natural Cell

Equilibrium between cell survival and death is important for normal cell homeostasis and development and also for inhibiting pathologies particularly cancer. Anastasis is a natural cell recovery phenomenon that rescues cells from the brink of death or a mechanism by which cells recuperate from apoptotic lesions and return to its normal active and functioning state. Programmed cell death (apoptosis) was known to be an intrinsically irreversible cascade that commits cells to a rapid destruction. However, recent studies have demonstrated the possibility of recovering dying cells even at the late stages. Anastasis uses the usual pro-metastatic and pro-survival factors to inhibit apoptotic progression. Epithelial mesenchymal transition (EMT) activation and its related modulators is not only linked with cellular metastasis and survivability but also widely associated with the stemness of cancer cells.

Programmed cell death in Drosophila

1994 ◽  
Vol 345 (1313) ◽  
pp. 247-250 ◽  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Large Fraction ◽  
X Ray ◽  
Large Numbers ◽  
Single Region ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
Dying Cells ◽  
Natural Cell

During Drosophila development, large numbers of cells undergo natural cell death. Even though the onset of these deaths is controlled by many different signals, most of the dying cells undergo common morphological and biochemical changes that are characteristic of apoptosis in vertebrates. We have surveyed a large fraction of the Drosophila genome for genes that are required for programmed cell death by examining the pattern of apoptosis in embryos homozygous for previously identified chromosomal deletions. A single region on the third chromosome (in position 75C1,2) was found to be essential for all cell deaths that normally occur during Drosophila embryogenesis. We have cloned the corresponding genomic DNA and isolated a gene, reaper , which is capable of restoring apoptosis when reintroduced into cell death defective deletions. The reaper gene is specifically expressed in cells that are doomed to die, and its expression precedes the first morphological signs of apoptosis by 1-2 h. This gene is also rapidly induced upon X-ray irradiation, and reaper deletions offer significant protection against radiation-induced apoptosis. Our results suggest that reaper represents a key regulatory switch for the activation of apoptosis in response to a variety of distinct signals.

scholarly journals Programmed cell death induced by high levels of cytokinin in Arabidopsis cultured cells is mediated by the cytokinin receptor CRE1/AHK4

2012 ◽  
Vol 63 (7) ◽  
pp. 2825-2832 ◽  
Author(s):  
M. Vescovi ◽  
M. Riefler ◽  
M. Gessuti ◽  
O. Novak ◽  
T. Schmulling ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cultured Cells ◽  
Cytokinin Receptor

Programmed cell death during Drosophila embryogenesis

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 29-43 ◽  
Author(s):  
J.M. Abrams ◽  
K. White ◽  
L.I. Fessler ◽  
H. Steller
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Acridine Orange ◽  
Nile Blue ◽  
Molecular Genetic ◽  
Blue Staining ◽  
Nuclear Condensation ◽  
The Central Nervous System ◽  
Ultrastructural Appearance ◽  
Dying Cells

The deliberate and orderly removal of cells by programmed cell death is a common phenomenon during the development of metazoan animals. We have examined the distribution and ultrastructural appearance of cell deaths that occur during embryogenesis in Drosophila melanogaster. A large number of cells die during embryonic development in Drosophila. These cells display ultrastructural features that resemble apoptosis observed in vertebrate systems, including nuclear condensation, fragmentation and engulfment by macrophages. Programmed cell deaths can be rapidly and reliably visualized in living wild-type and mutant Drosophila embryos using the vital dyes acridine orange or nile blue. Acridine orange appears to selectively stain apoptotic forms of death in these preparations, since cells undergoing necrotic deaths were not significantly labelled. Likewise, toluidine blue staining of fixed tissues resulted in highly specific labelling of apoptotic cells, indicating that apoptosis leads to specific biochemical changes responsible for the selective affinity to these dyes. Cell death begins at stage 11 (approximately 7 hours) of embryogenesis and thereafter becomes widespread, affecting many different tissues and regions of the embryo. Although the distribution of dying cells changes drastically over time, the overall pattern of cell death is highly reproducible for any given developmental stage. Detailed analysis of cell death in the central nervous system of stage 16 embryos (13-16 hours) revealed asymmetries in the exact number and position of dying cells on either side of the midline, suggesting that the decision to die may not be strictly predetermined at this stage. This work provides the basis for further molecular genetic studies on the control and execution of programmed cell death in Drosophila.

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.

Widespread programmed cell death in proliferative and postmitotic regions of the fetal cerebral cortex

Development ◽  
1996 ◽  
Vol 122 (4) ◽  
pp. 1165-1174 ◽  
Author(s):  
A.J. Blaschke ◽  
K. Staley ◽  
J. Chun
Keyword(s):  
Cell Death ◽  
Cerebral Cortex ◽  
Programmed Cell Death ◽  
Nuclear Dna ◽  
Temporal Distribution ◽  
Embryonic Cell ◽  
Postnatal Life ◽  
Neuron Development ◽  
Cortical Cells ◽  
Dying Cells

A key event in the development of the mammalian cerebral cortex is the generation of neuronal populations during embryonic life. Previous studies have revealed many details of cortical neuron development including cell birthdates, migration patterns and lineage relationships. Programmed cell death is a potentially important mechanism that could alter the numbers and types of developing cortical cells during these early embryonic phases. While programmed cell death has been documented in other parts of the embryonic central nervous system, its operation has not been previously reported in the embryonic cortex because of the lack of cell death markers and the difficulty in following the entire population of cortical cells. Here, we have investigated the spatial and temporal distribution of dying cells in the embryonic cortex using an in situ endlabelling technique called ‘ISEL+’ that identifies fragmented nuclear DNA in dying cells with increased sensitivity. The period encompassing murine cerebral cortical neurogenesis was examined, from embryonic days 10 through 18. Dying cells were rare at embryonic day 10, but by embryonic day 14, 70% of cortical cells were found to be dying. This number declined to 50% by embryonic day 18, and few dying cells were observed in the adult cerebral cortex. Surprisingly, while dying cells were observed throughout the cerebral cortical wall, the majority were found within zones of cell proliferation rather than in regions of postmitotic neurons. These observations suggest that multiple mechanisms may regulate programmed cell death in the developing cortex. Moreover, embryonic cell death could be an important factor enabling the selection of appropriate cortical cells before they complete their differentiation in postnatal life.

Thaxtomin A induces programmed cell death in Arabidopsis thaliana suspension-cultured cells

Planta ◽  
2005 ◽  
Vol 222 (5) ◽  
pp. 820-831 ◽  
Author(s):  
Isabelle Duval ◽  
Viviane Brochu ◽  
Mathieu Simard ◽  
Carole Beaulieu ◽  
Nathalie Beaudoin
Keyword(s):  
Arabidopsis Thaliana ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cultured Cells ◽  
Thaxtomin A ◽  
Suspension Cultured Cells

Metabolic events during programmed cell death in insect labial glands

1994 ◽  
Vol 72 (11-12) ◽  
pp. 597-601 ◽  
Author(s):  
Reginald Halaby ◽  
Zahra Zakeri ◽  
Richard A. Lockshin
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Acid Phosphatase ◽  
Programmed Cell Death ◽  
Manduca Sexta ◽  
Adenosine Triphosphate ◽  
Mitochondrial Respiration ◽  
Second Messengers ◽  
Labial Gland ◽  
Dying Cells

The labial gland of Manduca sexta is a valuable system to study the mechanisms of programmed cell death since the death of the gland is nearly synchronous and, except for the anterior duct, involves all of the tissue. The gland degenerates in 5 days during pupation. Our previous work documents a drop in total protein synthesis as the gland degenerates. To evaluate potential causes of this altered protein synthesis, we monitored several parameters of metabolism in dying cells: levels of adenosine triphosphate to estimate the energy resources of the gland; reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide to assess mitochondrial respiration; levels of acid phosphatase to assay lysosomal enzyme activity; and concentrations of cyclic nucleotides and inositol triphosphate to monitor signaling. While protein synthesis fell precipitously on day 0, total adenosine triphosphate and mitochondrial respiration were unchanged until the cells underwent massive collapse on day 3. Lysosomal acid phosphatase increased during early metamorphosis, and ultimately the bulk of the cytoplasm was destroyed in autophagic vacuoles. Changes in the concentrations of second messengers were modest and late. The relationships between the metabolism and the collapse of the labial gland are under investigation.Key words: programmed cell death, Manduca sexta, energetics, lysosomes, second messengers, protein synthesis.

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