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Journal articles on the topic 'Programmed cell death'

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Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.

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2

Roy, Jean-Michel. "Is programmed cell death a programmed death?" Biofutur 1998, no. 178 (May 1998): 12. http://dx.doi.org/10.1016/s0294-3506(98)80078-1.

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3

Lockshin, Richard A., and Zahra Zakeri. "Cell Death (Apoptosis, Programmed Cell Death)." Directions in Science 1 (February 27, 2002): 41–44. http://dx.doi.org/10.1100/tsw.2002.161.

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4

Fulton, Alice B. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.b.

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5

Novak, Jan. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.a.

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6

Novak, J., A. B. Fulton, and J. C. Ameisen. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 17–21. http://dx.doi.org/10.1126/science.274.5284.17c.

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7

Novak, J. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.

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8

Fulton, A. B. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20. http://dx.doi.org/10.1126/science.274.5284.20-a.

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9

Novak, J. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20a. http://dx.doi.org/10.1126/science.274.5284.20a.

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10

Fulton, A. B. "Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20b. http://dx.doi.org/10.1126/science.274.5284.20b.

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11

Woodle, E. Steve, and Sanjay Kulkarni. "PROGRAMMED CELL DEATH." Transplantation 66, no. 6 (September 1998): 681–91. http://dx.doi.org/10.1097/00007890-199809270-00001.

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12

RATEL, DAVID, SYLVIE BOISSEAU, VALÉRY NASSER, FRANÇOIS BERGER, and DIDIER WION. "Programmed Cell Death or Cell Death Programme? That is the Question." Journal of Theoretical Biology 208, no. 3 (February 2001): 385–86. http://dx.doi.org/10.1006/jtbi.2000.2218.

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13

Yao, Nan, and Jean T. Greenberg. "Arabidopsis ACCELERATED CELL DEATH2 Modulates Programmed Cell Death." Plant Cell 18, no. 2 (December 30, 2005): 397–411. http://dx.doi.org/10.1105/tpc.105.036251.

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14

Liu, Qiang, and Chun-Sheng Li. "Programmed Cell Death-1/Programmed Death-ligand 1 Pathway." Chinese Medical Journal 130, no. 8 (April 2017): 986–92. http://dx.doi.org/10.4103/0366-6999.204113.

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15

Speir, Mary, James E. Vince, and Thomas Naderer. "Programmed cell death inLegionellainfection." Future Microbiology 9, no. 1 (January 2014): 107–18. http://dx.doi.org/10.2217/fmb.13.139.

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16

Ameisen, J. C. "Response: Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20–21. http://dx.doi.org/10.1126/science.274.5284.20-b.

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17

Ameisen, J. C. "Response: Programmed Cell Death." Science 274, no. 5284 (October 4, 1996): 20c—21c. http://dx.doi.org/10.1126/science.274.5284.20c.

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18

Föller, Michael, Stephan M. Huber, and Florian Lang. "Erythrocyte programmed cell death." IUBMB Life 60, no. 10 (October 2008): 661–68. http://dx.doi.org/10.1002/iub.106.

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19

Kuan, Nai-Kang. "Apoptosis: Programmed Cell Death." Archives of Surgery 133, no. 7 (July 1, 1998): 773. http://dx.doi.org/10.1001/archsurg.133.7.773.

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20

Ondroušková, Eva, and Bořivoj Vojtěšek. "Programmed Cell Death in Cancer Cells." Klinicka onkologie 27, Suppl 1 (June 15, 2014): S7—S14. http://dx.doi.org/10.14735/amko20141s7.

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21

Jaafar, Jaafar, Eugenio Fernandez, Heba Alwan, and Jacques Philippe. "Programmed cell death-1 and programmed cell death ligand-1 antibodies-induced dysthyroidism." Endocrine Connections 7, no. 5 (May 2018): R196—R211. http://dx.doi.org/10.1530/ec-18-0079.

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Background Monoclonal antibodies blocking the programmed cell death-1 (PD-1) or its ligand (PD-L1) are a group of immune checkpoints inhibitors (ICIs) with proven antitumor efficacy. However, their use is complicated by immune-related adverse events (irAEs), including endocrine adverse events (eAEs). Purpose We review the incidence, time to onset and resolution rate of dysthyroidism induced by PD-1/PD-L1 Ab, and the clinical, biological and radiological findings. We aim to discuss the potential mechanisms of PD-1/PD-L1 Ab-induced dysthyroidism, and to propose a management algorithm. Methods We performed a literature search of available clinical trials regarding PD-1/PD-L1 Ab in the PubMed database. We selected all English language clinical trials that included at least 100 patients. We also present selected case series or reports, retrospective studies and reviews related to this issue. Findings In patients treated with PD-1 Ab, hypothyroidism occurred in 2–10.1% and hyperthyroidism occurred in 0.9–7.8%. When thyroiditis was reported separately, it occurred in 0.34–2.6%. Higher rates were reported when PD-1 Ab were associated with other ICI or chemotherapy. The median time to onset of hyperthyroidism and hypothyroidism after PD-1 Ab initiation was 23–45 days and 2–3.5 months, respectively. Regarding PD-L1 Ab, hypothyroidism occurred in 0–10% and hyperthyroidism in 0.5–2% of treated patients. The average time to onset of dysthyroidism after PD-L1 Ab was variable and ranged from 1 day after treatment initiation to 31 months. Conclusion Dysthyroidism occurs in up to 10% of patients treated with PD-1/PD-L1 Ab. Hypothyroidism and reversible destructive thyroiditis are the most frequent endocrine adverse events (eAE) in PD-1/PD-L1 treated patients. Immune and non-immune mechanisms are potentially involved, independently of the presence of thyroid antibodies.

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22

KOIKE, TATSURO. "Programmed cell death.Mainly on cell death." Kagaku To Seibutsu 30, no. 6 (1992): 380–84. http://dx.doi.org/10.1271/kagakutoseibutsu1962.30.380.

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23

Abrams, J. M., K. White, L. I. Fessler, and H. Steller. "Programmed cell death during Drosophila embryogenesis." Development 117, no. 1 (January 1, 1993): 29–43. http://dx.doi.org/10.1242/dev.117.1.29.

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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.

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24

Meier, Pascal, and John Silke. "Programmed cell death: Superman meets Dr Death." Nature Cell Biology 5, no. 12 (December 1, 2003): 1035–38. http://dx.doi.org/10.1038/ncb1203-1035.

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25

Williams, Thomas J., Luis E. Gonzales-Huerta, and Darius Armstrong-James. "Fungal-Induced Programmed Cell Death." Journal of Fungi 7, no. 3 (March 20, 2021): 231. http://dx.doi.org/10.3390/jof7030231.

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Fungal infections are a cause of morbidity in humans, and despite the availability of a range of antifungal treatments, the mortality rate remains unacceptably high. Although our knowledge of the interactions between pathogenic fungi and the host continues to grow, further research is still required to fully understand the mechanism underpinning fungal pathogenicity, which may provide new insights for the treatment of fungal disease. There is great interest regarding how microbes induce programmed cell death and what this means in terms of the immune response and resolution of infection as well as microbe-specific mechanisms that influence cell death pathways to aid in their survival and continued infection. Here, we discuss how programmed cell death is induced by fungi that commonly cause opportunistic infections, including Candida albicans, Aspergillus fumigatus, and Cryptococcus neoformans, the role of programmed cell death in fungal immunity, and how fungi manipulate these pathways.

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26

A Ali Azzwali, Abdu-Alhameed, and Azab Elsayed Azab. "Mechanisms of programmed cell death." Journal of Applied Biotechnology & Bioengineering 6, no. 4 (July 10, 2019): 156–58. http://dx.doi.org/10.15406/jabb.2019.06.00188.

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The present review aims to spotlight on the mechanisms and stages of programmed cell death. Apoptosis, known as programmed cell death, is a homeostatic mechanism that generally occurs during development and aging in order to keep cells in tissue. It can also act as a protective mechanism, for example, in immune response or if cells are damaged by toxin agents or diseases. In cancer treatment, drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway in cancer treatment, drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway. Corticosteroids can cause apoptotic death in a number of cells. A number of changes in cell morphology are related to the different stages of apoptosis, which includes nuclear DNA fragmentation, cell shrinkage, chromatin condensation, membrane blebbing, and the formation of apoptotic bodies. There are three pathways for apoptosis, the intrinsic (mitochondrial) and extrinsic (death receptor) are the two major paths that are interlinked and that can effect one another. Conclusion: It can be concluded that apoptosis is a homeostatic mechanism that generally occurs during development and aging in order to keep cells in tissue. Drugs and irradiation used in chemotherapy leads to DNA damage, which results in triggering apoptosis through the p53 dependent pathway. The apoptosis, stages are includes nuclear DNA fragmentation, cell shrinkage, chromatin condensation, membrane blebbing, and the formation of apoptotic bodies. There are three pathways for apoptosis.

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27

Cornillon, S., C. Foa, J. Davoust, N. Buonavista, J. D. Gross, and P. Golstein. "Programmed cell death in Dictyostelium." Journal of Cell Science 107, no. 10 (October 1, 1994): 2691–704. http://dx.doi.org/10.1242/jcs.107.10.2691.

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Programmed cell death (PCD) of Dictyostelium discoideum cells was triggered precisely and studied quantitatively in an in vitro system involving differentiation without morphogenesis. In temporal succession after the triggering of differentiation, PCD included first an irreversible step leading to the inability to regrow at 8 hours. At 12 hours, massive vacuolisation was best evidenced by confocal microscopy, and prominent cytoplasmic condensation and focal chromatin condensation could be observed by electron microscopy. Membrane permeabilization occurred only very late (at 40–60 hours) as judged by propidium iodide staining. No early DNA fragmentation could be detected by standard or pulsed field gel electrophoresis. These traits exhibit some similarity to those of previously described non-apoptotic and apoptotic PCD, suggesting the hypothesis of a single core molecular mechanism of PCD emerging in evolution before the postulated multiple emergences of multicellularity. A single core mechanism would underly phenotypic variations of PCD resulting in various cells from differences in enzymatic equipment and mechanical constraints. A prediction is that some of the molecules involved in the core PCD mechanism of even phylogenetically very distant organisms, e.g. Dictyostelium and vertebrates, should be related.

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28

Shimamoto, Ko, Akira Takahashi, Kenji Henmi, Eiichiro Ono, Satoru Hatakeyama, Megumi Iwano, and Tsutomu Kawasaki. "Programmed Cell Death in Plants." Plant Biotechnology 16, no. 1 (1999): 49–53. http://dx.doi.org/10.5511/plantbiotechnology.16.49.

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29

Conradt, Barbara, Yi-Chun Wu, and Ding Xue. "Programmed Cell Death DuringCaenorhabditis elegansDevelopment." Genetics 203, no. 4 (August 2016): 1533–62. http://dx.doi.org/10.1534/genetics.115.186247.

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30

Hochman, Ayala. "Programmed Cell Death in Prokaryotes." Critical Reviews in Microbiology 23, no. 3 (January 1997): 207–14. http://dx.doi.org/10.3109/10408419709115136.

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31

Martin, Seamus J. "Programmed Cell Death and AIDS." Science 262, no. 5138 (November 26, 1993): 1355–56. http://dx.doi.org/10.1126/science.262.5138.1355.b.

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32

Ames, Elizabeth G., and Jess G. Thoene. "Programmed Cell Death in Cystinosis." Cells 11, no. 4 (February 15, 2022): 670. http://dx.doi.org/10.3390/cells11040670.

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Cystinosis is a lethal autosomal recessive disease that has been known clinically for over 100 years. There are now specific treatments including dialysis, renal transplantation and the orphan drug, cysteamine, which greatly improve the duration and quality of patient life, however, the cellular mechanisms responsible for the phenotype are unknown. One cause, programmed cell death, is clearly involved. Study of extant literature via Pubmed on “programmed cell death” and “apoptosis” forms the basis of this review. Most of such studies involved apoptosis. Numerous model systems and affected tissues in cystinosis have shown an increased rate of apoptosis that can be partially reversed with cysteamine. Proposed mechanisms have included changes in protein signaling pathways, autophagy, gene expression programs, and oxidative stress.

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33

Martin, Seamus J. "Programmed Cell Death and AIDS." Science 262, no. 5138 (November 26, 1993): 1355–56. http://dx.doi.org/10.1126/science.262.5138.1355-b.

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34

Moschou, P. N., and K. A. Roubelakis-Angelakis. "Polyamines and programmed cell death." Journal of Experimental Botany 65, no. 5 (November 11, 2013): 1285–96. http://dx.doi.org/10.1093/jxb/ert373.

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35

Dangler, C. A. "Book Review: Programmed Cell Death." Veterinary Pathology 37, no. 1 (January 2000): 108. http://dx.doi.org/10.1354/vp.37-1-108.

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36

Sun, Y., and Z.-L. Peng. "Programmed cell death and cancer." Postgraduate Medical Journal 85, no. 1001 (March 1, 2009): 134–40. http://dx.doi.org/10.1136/pgmj.2008.072629.

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37

Fomicheva, A. S., A. I. Tuzhikov, R. E. Beloshistov, S. V. Trusova, R. A. Galiullina, L. V. Mochalova, N. V. Chichkova, and A. B. Vartapetian. "Programmed cell death in plants." Biochemistry (Moscow) 77, no. 13 (December 2012): 1452–64. http://dx.doi.org/10.1134/s0006297912130044.

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38

Popov, L. S., and L. I. Korochkin. "Apoptosis: Genetically Programmed Cell Death." Russian Journal of Genetics 40, no. 2 (February 2004): 99–113. http://dx.doi.org/10.1023/b:ruge.0000016982.08548.9f.

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39

van den Bergh, Walter M. "Disturbing the Programmed Cell Death*." Critical Care Medicine 41, no. 9 (September 2013): 2250–51. http://dx.doi.org/10.1097/ccm.0b013e31828e90b9.

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40

Martin, S. J. "Programmed Cell Death and AIDS." Science 262, no. 5138 (November 26, 1993): 1355–56. http://dx.doi.org/10.1126/science.262.5138.1355-a.

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41

Lee, H. P. "Programmed cell death in placentas." Placenta 19, no. 7 (September 1998): A9. http://dx.doi.org/10.1016/s0143-4004(98)91078-5.

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42

Martin, S. "Programmed cell death and AIDS." Science 262, no. 5138 (November 26, 1993): 1355. http://dx.doi.org/10.1126/science.7902613.

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43

BAGCHI, SUSMITA, ABRAHAM E. ONIKU, KATE TOPPING, ZAHRA N. MAMHOUD, and TIMOTHY A. PAGET. "Programmed cell death in Giardia." Parasitology 139, no. 7 (March 12, 2012): 894–903. http://dx.doi.org/10.1017/s003118201200011x.

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SUMMARYProgrammed cell death (PCD) has been observed in many unicellular eukaryotes; however, in very few cases have the pathways been described. Recently the early divergent amitochondrial eukaryote Giardia has been included in this group. In this paper we investigate the processes of PCD in Giardia. We performed a bioinformatics survey of Giardia genomes to identify genes associated with PCD alongside traditional methods for studying apoptosis and autophagy. Analysis of Giardia genomes failed to highlight any genes involved in apoptotic-like PCD; however, we were able to induce apoptotic-like morphological changes in response to oxidative stress (H2O2) and drugs (metronidazole). In addition we did not detect caspase activity in induced cells. Interestingly, we did observe changes resembling autophagy when cells were starved (staining with MDC) and genome analysis revealed some key genes associated with autophagy such as TOR, ATG1 and ATG 16. In organisms such as Trichomonas vaginalis, Entamoeba histolytica and Blastocystis similar observations have been made but no genes have been identified. We propose that Giardia possess a pathway of autophagy and a form of apoptosis very different from the classical known mechanism; this may represent an early form of programmed cell death.

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44

McCall, Kimberly. "Programmed cell death in development." Seminars in Cell & Developmental Biology 16, no. 2 (April 2005): 213. http://dx.doi.org/10.1016/j.semcdb.2005.01.001.

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45

Cookson, Brad T., and Molly A. Brennan. "Pro-inflammatory programmed cell death." Trends in Microbiology 9, no. 3 (March 2001): 113–14. http://dx.doi.org/10.1016/s0966-842x(00)01936-3.

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46

Miyairi, Isao, and Gerald I. Byrne. "Chlamydia and programmed cell death." Current Opinion in Microbiology 9, no. 1 (February 2006): 102–8. http://dx.doi.org/10.1016/j.mib.2005.12.004.

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47

Welburn, S. C., M. A. Barcinski, and G. T. Williams. "Programmed cell death in trypanosomatids." Parasitology Today 13, no. 1 (January 1997): 22–26. http://dx.doi.org/10.1016/s0169-4758(96)10076-4.

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48

Hengartner, Michael O. "Programmed cell death in invertebrates." Current Opinion in Genetics & Development 6, no. 1 (February 1996): 34–38. http://dx.doi.org/10.1016/s0959-437x(96)90007-6.

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49

Steller, Hermann, and Megan E. Grether. "Programmed cell death in Drosophila." Neuron 13, no. 6 (December 1994): 1269–74. http://dx.doi.org/10.1016/0896-6273(94)90413-8.

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50

Yamaguchi, Yoshifumi, and Masayuki Miura. "Programmed Cell Death in Neurodevelopment." Developmental Cell 32, no. 4 (February 2015): 478–90. http://dx.doi.org/10.1016/j.devcel.2015.01.019.

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