scholarly journals Сell death and its significance in reproductive pathology

2021 ◽  
Vol 4 (2) ◽  
pp. 18-26
Author(s):  
M. M. Zhelavskyi ◽  
S. P. Kernychnyi ◽  
O. Ya. Dmytriv
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Biology ◽  
Apoptotic Cell ◽  
Clinical Aspects ◽  
Cellular Regulation ◽  
Cellular Mechanisms ◽  
Programmed Aging ◽  
Living Organisms ◽  
Reproductive Pathology

Since the middle of the last century, scientists have been interested in the mechanisms of regulation of cell division, differentiation and aging of cells. The first objects of study were insects, helminths and other living organisms. From the very beginning, in the biology of cell development and regulation, scientists have attached leading importance to genetic factors. Later, more and more experience was gained on the influence of intracellular factors, metabolic changes and exogenous pathogens on the programmed cell death. Recent research on cell biology and pathology has focused on the study of apoptosis. The first described phenomenon of programmed cell death was apoptosis. Subsequent studies were aimed at the study programmed cell death. This review will provide an opportunity to consider the biological mechanisms of programmed cell death, differences and species characteristics. The author described the clinical aspects of apoptosis, necroptosis and pyroptosis and their importance in the formation of cellular homeostasis. In the present review article simple classification system, where the cell death entities are primarily categorized into programmed cell death. Multiple mechanisms and phenotypes compose programmed non-apoptotic cell death, including: autophagy, entosis, methuosis and paraptosis, mitoptosis and parthanatos, ferroptosis, pyroptosis NETosis and necroptosis. Changes of cellular regulation at development of pathologies at people and animals are considered. Cell biology includes a variety of mechanisms of programmed aging and death. Modern research is aimed at deepening the study multiple mechanisms and phenotypes compose programmed. Cells. will certainly be taken into account by the Nomenclature Committee on Cell Death. Cellular regulation is associated with a variety of physiological mechanisms of development, and is also important in processes such as inflammation, immune response, embryogenesis maintenance of tissue homeostasis. Study of factors of influence and mechanisms of regulation of aging of cells opens a curtain for development of the newest means of diagnostics of pathologies and development of pharmacological means for correction of cellular mechanisms at development of pathologies.

scholarly journals miR-103 Functions as a Tumor Suppressor by Directly Targeting Programmed Cell Death 10 in NSCLC

2018 ◽  
Vol 26 (4) ◽  
pp. 519-528 ◽  
Author(s):  
Dong Yang ◽  
Jian-Jun Wang ◽  
Jin-Song Li ◽  
Qian-Yu Xu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Tumor Size ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Invasion And Migration ◽  
Metastatic Capacity ◽  
And Migration

Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. Absence of miR-103 has recently been identified to be associated with metastatic capacity of primary lung tumors. However, the exact role of miR-103 in NSCLC and the molecular mechanism are unclear. In the present study, we showed that miR-103 expression was reduced in NSCLC tissues and cells. miR-103 expression was negatively correlated with tumor size and stage. The overall survival was longer in patients with higher miR-103 level than in those with lower miR-103 expression. miR-103 inhibited cell proliferation in A549 cells, decreased tumor weight and volume, and prolonged survival of tumor-implanted nude mice. miR-103 increased apoptotic cell death in A549 cells. Furthermore, miR-103 decreased the invasion and migration abilities in A549 cells, as evidenced by Transwell and wound healing results. Downregulation of miR-103 significantly reduced the level of programmed cell death 10 (PDCD10). We found a significant decrease in the relative luciferase activity of the reporter gene in A549 cells cotransfected with the miR-103 mimic and pGL3-PDCD10 WT 3′-UTR, but not pGL3-PDCD10 mut 3′-UTR. We showed that overexpression of PDCD10 significantly inhibited miR-103-induced inhibition of cell proliferation, increased apoptosis, and decreased invasion and migration in A549 cells. Moreover, we found that PDCD10 expression was increased in NSCLC tissues and cells. PDCD10 expression was positively correlated with tumor size and stage. Overexpression of PDCD10 increased cell proliferation and inhibited apoptosis in A549 cells. The data demonstrated that dysregulation of the miR-103/PDCD10 signal may be a novel therapeutic target for the treatment of NSCLC.

scholarly journals Role of Ced-3/ICE-family proteases in staurosporine-induced programmed cell death.

1996 ◽  
Vol 133 (5) ◽  
pp. 1041-1051 ◽  
Author(s):  
M D Jacobsen ◽  
M Weil ◽  
M C Raff
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mammalian Cell ◽  
Mammalian Cells ◽  
Apoptotic Cell ◽  
Interleukin 1 ◽  
Cell Types ◽  
Cysteine Proteases ◽  
A Cell ◽  
Bona Fide

In the accompanying paper by Weil et al. (1996) we show that staurosporine (STS), in the presence of cycloheximide (CHX) to inhibit protein synthesis, induces apoptotic cell death in a large variety of nucleated mammalian cell types, suggesting that all nucleated mammalian cells constitutively express all of the proteins required to undergo programmed cell death (PCD). The reliability of that conclusion depends on the evidence that STS-induced, and (STS + CHS)-induced, cell deaths are bona fide examples of PCD. There is rapidly accumulating evidence that some members of the Ced-3/Interleukin-1 beta converting enzyme (ICE) family of cysteine proteases are part of the basic machinery of PCD. Here we show that Z-Val-Ala-Asp-fluoromethylketone (zVAD-fmk), a cell-permeable, irreversible, tripeptide inhibitor of some of these proteases, suppresses STS-induced and (STS + CHX)-induced cell death in a wide variety of mammalian cell types, including anucleate cytoplasts, providing strong evidence that these are all bona fide examples of PCD. We show that the Ced-3/ICE family member CPP32 becomes activated in STS-induced PCD, and that Bcl-2 inhibits this activation. Most important, we show that, in some cells at least, one or more CPP32-family members, but not ICE itself, is required for STS-induced PCD. Finally, we show that zVAD-fmk suppresses PCD in the interdigital webs in developing mouse paws and blocks the removal of web tissue during digit development, suggesting that this inhibition will be a useful tool for investigating the roles of PCD in various developmental processes.

Masterminds or minions? Cysteine proteinases in plant programmed cell deathThis review is one of a selection of papers published in the Special Issue on Plant Cell Biology.

2006 ◽  
Vol 84 (4) ◽  
pp. 651-667 ◽  
Author(s):  
Christopher P. Trobacher ◽  
Adriano Senatore ◽  
John S. Greenwood
Keyword(s):  
Cell Death ◽  
Cell Biology ◽  
Apoptotic Cell ◽  
Gene Families ◽  
Cysteine Proteinases ◽  
Special Issue ◽  
Multicellular Organisms ◽  
Protease Expression ◽  
Signalling Cascade ◽  
Selection Of

Cysteine proteinases are ubiquitously involved in programmed cell death (PCD) in multicellular organisms. In animals, one group of cysteine proteinases, the cysteine-dependent aspartate-specific proteinases (caspases), are involved in a proteolytic signalling cascade that controls apoptosis, the most studied form of PCD. The enzymes act as both masterminds and executioners in apoptotic cell death. In plants, members of the metacaspase family, as well as those of the papain-like and legumain families, of cysteine proteinases have all been implicated in PCD. These enzymes often belong to sizeable gene families, with Arabidopsis having 9 metacaspase, 32 papain-like, and 4 legumain genes. This redundancy has made it difficult to ascertain the functional importance of any particular enzyme in plant PCD, as many are often expressed in a given tissue undergoing PCD. As yet, mechanisms similar to the apoptotic caspase cascade in animals have not been uncovered in plants and, indeed, may not exist. Are the various cysteine proteinases, so often implicated in plant PCD, merely acting as minions in the process? This review will outline reports of cysteine proteinases associated with plant PCD, discuss problems in determining the function of specific proteases, and suggest avenues for determining how these enzymes might be regulated and how PCD pathways upstream of protease expression and activation might operate.

scholarly journals I Spy in the Developing Fly a Multitude of Ways to Die

2018 ◽  
Vol 6 (4) ◽  
pp. 26 ◽  
Author(s):  
Alla Yalonetskaya ◽  
Albert Mondragon ◽  
Johnny Elguero ◽  
Kimberly McCall
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Nervous System ◽  
Programmed Cell Death ◽  
Apoptotic Cell ◽  
Model Organism ◽  
Cell Numbers ◽  
Genetic Techniques ◽  
Developmental Cell Death ◽  
Different Tissues

Cell proliferation and cell death are two opposing, yet complementary fundamental processes in development. Cell proliferation provides new cells, while developmental programmed cell death adjusts cell numbers and refines structures as an organism grows. Apoptosis is the best-characterized form of programmed cell death; however, there are many other non-apoptotic forms of cell death that occur throughout development. Drosophila is an excellent model for studying these varied forms of cell death given the array of cellular, molecular, and genetic techniques available. In this review, we discuss select examples of apoptotic and non-apoptotic cell death that occur in different tissues and at different stages of Drosophila development. For example, apoptosis occurs throughout the nervous system to achieve an appropriate number of neurons. Elsewhere in the fly, non-apoptotic modes of developmental cell death are employed, such as in the elimination of larval salivary glands and midgut during metamorphosis. These and other examples discussed here demonstrate the versatility of Drosophila as a model organism for elucidating the diverse modes of programmed cell death.

Cell biology and programmed cell death in MDS

1994 ◽  
Vol 18 ◽  
pp. 5 ◽  
Author(s):  
Yataro Yoshida ◽  
Hiroshi Kawabata ◽  
Naoyuki Anzai
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Biology

scholarly journals Investigating Programmed Cell Death and Tumor Invasion in a Three-Dimensional (3D) Microfluidic Model of Glioblastoma

2020 ◽  
Vol 21 (9) ◽  
pp. 3162
Author(s):  
Ehsan Samiei ◽  
Amir Seyfoori ◽  
Brian Toyota ◽  
Saeid Ghavami ◽  
Mohsen Akbari
Keyword(s):  
Cell Death ◽  
Survival Rate ◽  
Programmed Cell Death ◽  
Tumor Invasion ◽  
3D Model ◽  
Apoptotic Cell ◽  
Simultaneous Detection ◽  
Three Dimensional ◽  
Drug Induced ◽  
Induced Apoptosis

Glioblastoma multiforme (GBM) is a rapidly progressive and deadly form of brain tumor with a median survival rate of ~15 months. GBMs are hard to treat and significantly affect the patient’s physical and cognitive abilities and quality of life. Temozolomide (TMZ)—an alkylating agent that causes DNA damage—is the only chemotherapy choice for the treatment of GBM. However, TMZ also induces autophagy and causes tumor cell resistance and thus fails to improve the survival rate among patients. Here, we studied the drug-induced programmed cell death and invasion inhibition capacity of TMZ and a mevalonate cascade inhibitor, simvastatin (Simva), in a three-dimensional (3D) microfluidic model of GBM. We elucidate the role of autophagy in apoptotic cell death by comparing apoptosis in autophagy knockdown cells (Atg7 KD) against their scrambled counterparts. Our results show that the cells were significantly less sensitive to drugs in the 3D model as compared to monolayer culture systems. An immunofluorescence analysis confirmed that apoptosis is the mechanism of cell death in TMZ- and Simva-treated glioma cells. However, the induction of apoptosis in the 3D model is significantly lower than in monolayer cultures. We have also shown that autophagy inhibition (Atg7 KD) did not change TMZ and Simva-induced apoptosis in the 3D microfluidic model. Overall, for the first time in this study we have established the simultaneous detection of drug induced apoptosis and autophagy in a 3D microfluidic model of GBM. Our study presents a potential ex vivo platform for developing novel therapeutic strategies tailored toward disrupting key molecular pathways involved in programmed cell death and tumor invasion in glioblastoma.

scholarly journals Activation-induced T-cell death is cell cycle dependent and regulated by cyclin B.

1995 ◽  
Vol 15 (2) ◽  
pp. 932-942 ◽  
Author(s):  
R Fotedar ◽  
J Flatt ◽  
S Gupta ◽  
R L Margolis ◽  
P Fitzgerald ◽  
...  
Keyword(s):  
Cell Cycle ◽  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Programmed Cell Death ◽  
Kinase Activity ◽  
Apoptotic Cell ◽  
Cyclin B ◽  
Activation Induced Cell Death ◽  
Diagnostic Characteristics

Developing thymocytes and some T-cell hybridomas undergo activation-dependent programmed cell death. Although recent studies have identified some critical regulators in programmed cell death, the role of cell cycle regulation in activation-induced cell death in T cells has not been addressed. We demonstrate that synchronized T-cell hybridomas, irrespective of the point in the cell cycle at which they are activated, stop cycling shortly after they reach G2/M. These cells exhibit the diagnostic characteristics of apoptotic cell death. Although p34cdc2 levels are not perturbed after activation of synchronously cycling T cells, cyclin B- and p34cdc2-associated histone H1 kinase activity is persistently elevated. This activation-dependent induction of H1 kinase activity in T cells is associated with a decrease in the phosphotyrosine content of p34cdc2. We also demonstrate that transient inappropriate coexpression of cyclin B with p34cdc2 induces DNA fragmentation in a heterologous cell type. Finally, in T cells, cyclin B-specific antisense oligonucleotides suppress activation-induced cell death but not cell death induced by exposure to dexamethasone. We therefore conclude that a persistent elevation of the level of cyclin B kinase is required for activation-induced programmed T-cell death.

scholarly journals Programmed Cell Death Not as Sledgehammer but as Chisel: Apoptosis in Normal and Abnormal Craniofacial Patterning and Development

2021 ◽  
Vol 9 ◽  
Author(s):  
Claudia Compagnucci ◽  
Kira Martinus ◽  
John Griffin ◽  
Michael J. Depew
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Neural Crest ◽  
Congenital Malformations ◽  
Apoptotic Cell ◽  
Clinical Importance ◽  
Craniofacial Development ◽  
Epithelial Morphogenesis ◽  
Upper Jaw

Coordination of craniofacial development involves an complex, intricate, genetically controlled and tightly regulated spatiotemporal series of reciprocal inductive and responsive interactions among the embryonic cephalic epithelia (both endodermal and ectodermal) and the cephalic mesenchyme — particularly the cranial neural crest (CNC). The coordinated regulation of these interactions is critical both ontogenetically and evolutionarily, and the clinical importance and mechanistic sensitivity to perturbation of this developmental system is reflected by the fact that one-third of all human congenital malformations affect the head and face. Here, we focus on one element of this elaborate process, apoptotic cell death, and its role in normal and abnormal craniofacial development. We highlight four themes in the temporospatial elaboration of craniofacial apoptosis during development, namely its occurrence at (1) positions of epithelial-epithelial apposition, (2) within intra-epithelial morphogenesis, (3) during epithelial compartmentalization, and (4) with CNC metameric organization. Using the genetic perturbation of Satb2, Pbx1/2, Fgf8, and Foxg1 as exemplars, we examine the role of apoptosis in the elaboration of jaw modules, the evolution and elaboration of the lambdoidal junction, the developmental integration at the mandibular arch hinge, and the control of upper jaw identity, patterning and development. Lastly, we posit that apoptosis uniquely acts during craniofacial development to control patterning cues emanating from core organizing centres.

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