Mitochondrial apoptotic pathways induced by Drosophila programmed cell death regulators

2003 ◽  
Vol 304 (3) ◽  
pp. 531-537 ◽  
Author(s):  
Cristina Claverı́a ◽  
Miguel Torres
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Apoptotic Pathways

Beyond apoptosis: nonapoptotic cell death in physiology and disease

2005 ◽  
Vol 83 (5) ◽  
pp. 579-588 ◽  
Author(s):  
Claudio A Hetz ◽  
Vicente Torres ◽  
Andrew F.G Quest
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Death Receptor ◽  
Receptor Signaling ◽  
Family Analysis ◽  
Caspase Family ◽  
Death Receptor Signaling ◽  
Apoptotic Pathways ◽  
Nonapoptotic Cell Death ◽  
High Degree

Apoptosis is a morphologically defined form of programmed cell death (PCD) that is mediated by the activation of members of the caspase family. Analysis of death-receptor signaling in lymphocytes has revealed that caspase-dependent signaling pathways are also linked to cell death by nonapoptotic mechanisms, indicating that apoptosis is not the only form of PCD. Under physiological and pathological conditions, cells demonstrate a high degree of flexibility in cell-death responses, as is reflected in the existence of a variety of mechanisms, including necrosis-like PCD, autophagy (or type II PCD), and accidental necrosis. In this review, we discuss recent data suggesting that canonical apoptotic pathways, including death-receptor signaling, control caspase-dependent and -independent cell-death pathways.Key words: apoptosis, necrosis, nonapoptotic programmed cell death, death receptors, ceramides.

scholarly journals Neuronal apoptosis: signal and cell diversity

1969 ◽  
Vol 40 (1) ◽  
pp. 124-133
Author(s):  
Lina Vanessa Becerra ◽  
Hernán José Pimienta
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Neuronal Response ◽  
Neuronal Cell ◽  
Cell Types ◽  
Point Of View ◽  
Trophic Factors ◽  
Cell Diversity ◽  
Apoptotic Pathways ◽  
The Brain

Programmed cell death occurs as a physiological process during development. In the brain and spinal cord this event determines the number and location of the different cell types. In adulthood, programmed cell death or apoptosis is more restricted but it may play a major role in different acute and chronic pathological entities. However, in contrast to other tissues where apoptosis has been widely documented from a morphological point of view, in the central nervous system complete anatomical evidence of apoptosis is scanty. In spite of this there is consensus about the activation of different signal systems associated to programmed cell death. In the present article we attempt to summarize the main apoptotic pathways so far identified in nervous tissue. Considering that apoptotic pathways are multiple, the neuronal cell types are highly diverse and specialized and that neuronal response to injury and survival depends upon tissue context, (i.e., preservation of connectivity, glial integrity and cell matrix, blood supply and trophic factors availability) what is relevant for the apoptotic process in a sector of the brain may not be important in another.

scholarly journals EXPERIMENTAL MODELING OF APOPTOSIS UNDER CONDITIONS OF STABLE STRONTIUM EXPOSURE

2019 ◽  
Vol 21 (1) ◽  
pp. 137-140
Author(s):  
O. V. Dolgikh ◽  
N. V. Zaitseva ◽  
D. G. Dianova ◽  
A. V. Krivtsov ◽  
K. D. Starkova ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Annexin V ◽  
Fold Increase ◽  
Apoptosis Markers ◽  
Stable Strontium ◽  
Cell Death Mechanisms ◽  
Apoptotic Pathways ◽  
And Control

Apoptosis is defined as a highly regulated form of programmed cell death with typical morphological and biochemical features. A variety of factors, including heavy metals, may influence the intensity of programmed cell death. The aim of the work was to simulate apoptosis in an in vitrosystem under the conditions of stable strontium exposure. The children’s population consuming drinking water with high strontium (Sr2+) content (n = 49) was observed. The level of lymphocyte apoptosis was determined with flow cytometry technique, by means of labeled annexin V-FITC conjugate (AnnV-FITC) and propidium iodide (PI) staining. AnnV-FITC+PI- cells were regarded as early apoptotic forms, whereas late apoptotic and/or necrotic cells were AnnV-FITC+PI+. The isolated leukocytes were incubated with Sr2+ at a concentration of 7.0 mg/l, the maximal permitted concentration (MPC) for water of aqueous objects, for 4 hours at 37 ºC. Expression of CD95 and p53 apoptosis markers was performed by flow cytometry using labeled monoclonal antibodies.In vitroexposure to strontium was associated with significantly decreased expression of apoptosisregulating factors, i.e., membrane marker CD95 and intracellular transcription protein p53, 1.56- and 1.68-fold, respectively. Meanwhile, we revealed a significantly (4.68-fold) decreased amounts of AnnV-FITC+PI--cells, as well as a statistically significant (1.35-fold) increase of the AnnV-FITC+PI+-cells. Moreover, the amounts of AnnV-FITC+ PI--lymphocytes in all samples were below the physiological ranges and control values. The number of samples with higher contents of AnnV-FITC+PI+-lymphocyte exceeding the established standards and control values, was 30.8%. Thus, it has been experimentally proven that strontium, at a concentration corresponding to MPC for water objects may significantly inhibit cell death along apoptotic pathways, with switching to necrotic cell death mechanisms, according to phosphatidylserine contents, as detected by annexin V binding test. The data have revealed an ability of strontium to have a significant effect upon the parameters of regulation and maintenance of cellular homeostasis, by influencing the apoptosis intensity, due to shifting a balance towards necrosis and reducing expression of apoptosis-regulating factors. The results of this study may be used in order to identify some marker indexes of immune disorders potentially induced by external influence of strontium upon human health under specific environmental factors.

scholarly journals Flagellin/TLR5 responses in epithelia reveal intertwined activation of inflammatory and apoptotic pathways

2006 ◽  
Vol 290 (1) ◽  
pp. G96-G108 ◽  
Author(s):  
Hui Zeng ◽  
Huixia Wu ◽  
Valerie Sloane ◽  
Rheinallt Jones ◽  
Yimin Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Programmed Cell Death ◽  
Pathogenic Bacteria ◽  
Caspase Activation ◽  
Extrinsic Pathway ◽  
Tnf Α ◽  
Proinflammatory Responses ◽  
Apoptotic Pathways ◽  
Toll Like Receptor 5

Flagellin, the primary structural component of bacterial flagella, is recognized by Toll-like receptor 5 (TLR5) present on the basolateral surface of intestinal epithelial cells. Utilizing biochemical assays of proinflammatory signaling pathways and mRNA expression profiling, we found that purified flagellin could recapitulate the human epithelial cell proinflammatory responses activated by flagellated pathogenic bacteria. Flagellin-induced proinflammatory activation showed similar kinetics and gene specificity as that induced by the classical endogenous proinflammatory cytokine TNF-α, although both responses were more rapid than that elicited by viable flagellated bacteria. Flagellin, like TNF-α, activated a number of antiapoptotic mediators, and pretreatment of epithelial cells with this bacterial protein could protect cells from subsequent bacterially mediated apoptotic challenge. However, when NF-κB-mediated or phosphatidylinositol 3-kinase/Akt proinflammatory signaling was blocked, flagellin could induce programmed cell death. Consistently, we demonstrate that flagellin and viable flagellate Salmonella induces both the extrinsic and intrinsic caspase activation pathways, with the extrinsic pathway (caspase 8) activated by purified flagellin in a TLR5-dependant fashion. We conclude that interaction of flagellin with epithelial cells induces caspase activation in parallel with proinflammatory responses. Such intertwining of proinflammatory and apoptotic signaling mediated by bacterial products suggests roles for host programmed cell death in the pathogenesis of enteric infections.

scholarly journals Disturbances in the Mechanism of Apoptosis as One of the Causes of the Development of Cancer Diseases

2020 ◽  
Vol 18 (4) ◽  
pp. 63-73
Author(s):  
Paweł Rusin ◽  
Karolina Jabłońska
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Death Receptor ◽  
The Body ◽  
Stress Factors ◽  
Cancerous Cell ◽  
Anticancer Treatment ◽  
Apoptotic Pathways ◽  
Apoptosis Regulation ◽  
Multicellular Organisms

Apoptosis is a genetically programmed process that affects all multicellular organisms. This mechanism of programmed cell death is designed to protect the body against uncontrolled proliferation of cells with impaired functions. Apoptosis can occur through two major pathways. The extrinsic, initiated by signals from the death receptor, and the intrinsic one, resulting from a change in the permeability of the external mitochondrial membrane due to stress factors promoting the initiation of programmed cell death. Apoptosis may be influenced by many factors that may lead to suppressing the initiation of apoptotic pathways, and the damaged cell will develop, divide, and over time transform into a cancerous cell. As a result, cancer cells will be resistant to the applied chemo- and radiotherapy. The mechanisms responsible for apoptosis regulation are impaired, what eliminates the effects of therapies aimed at initiating this type of cell death. New types of molecular therapies provide an opportunity to increase the effectiveness of anticancer treatment, aiming at deficient proteins and suppressing or eliminating their antiapoptotic effects.

scholarly journals Conventional calpains and programmed cell death.

2011 ◽  
Vol 58 (3) ◽  
Author(s):  
Paulina Łopatniuk ◽  
Jacek M Witkowski
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
System Development ◽  
Cysteine Proteases ◽  
Drug Induced ◽  
Calcium Dependent ◽  
Immune System Development ◽  
Apoptotic Pathways ◽  
Induced Apoptosis ◽  
And Function

The evidence on the crucial role of a family of calcium-dependent cysteine proteases called calpains in programmed cell death is rich and still growing. However, understanding of the mechanisms of their functions in apoptosis is not full yet. Calpains have been implicated in both physiological and pathological cell death control, especially in various malignancies, but also in the immune system development and function. There is also growing evidence on calpain involvement in apoptosis execution in certain pathological conditions of the central nervous system, in cardiovascular diseases, etc. Understanding of the clinical significance of calpain activation pathways, after intense studies of the influence of calpain activity on drug-induced apoptosis, seems especially important lately, as calpains have become noticed as potential therapeutic targets. To allow pharmacological targeting of these enzymes, thorough knowledge of their patterns of activation and further interactions with already known apoptotic pathways is necessary. A comprehensive summary of both well established and recently obtained information in the field is an important step that may lead to future advances in the use of calpain-targeted agents in the clinic.

scholarly journals A time to kill: viral manipulation of the cell death program

2002 ◽  
Vol 83 (7) ◽  
pp. 1547-1564 ◽  
Author(s):  
Stewart Hay ◽  
George Kannourakis
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mechanisms Of Action ◽  
Host Cells ◽  
Viral Gene ◽  
Gene Products ◽  
Great Opportunity ◽  
Apoptotic Death ◽  
Cell Death Program ◽  
Apoptotic Pathways

Many viruses have as part of their arsenal the ability to modulate the apoptotic pathways of the host. It is counter-intuitive that such simple organisms would be efficient at regulating this the most crucial pathway within the host, given the relative complexity of the host cells. Yet, viruses have the potential to initiate or stay the onset of programmed cell death through the manipulation of a variety of key apoptotic proteins. It is the intention of this review to provide an overview of viral gene products that are able to promote or inhibit apoptotic death of the host cell and to discuss their mechanisms of action. It is not until recently that the depth at which viruses exploit the apoptotic pathways of their host has been seen. This understanding may provide a great opportunity for future therapeutic ventures.

scholarly journals Understanding and Targeting Apoptotic Pathways in Ovarian Cancer

Cancers ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 1631 ◽  
Author(s):  
Linah F. Al-Alem ◽  
Andrew T. Baker ◽  
Unnati M. Pandya ◽  
Eric L. Eisenhauer ◽  
Bo R. Rueda
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance ◽  
Cell Death ◽  
Immune System ◽  
Programmed Cell Death ◽  
Ovarian Cancer Cells ◽  
Cell Type ◽  
Apoptotic Pathways ◽  
External Forces ◽  
Multiple Signaling

Ovarian cancer cells evade the immune system as well as chemotherapeutic and/or biologic treatments through inherent or acquired mechanisms of survival and drug resistance. Depending on the cell type and the stimuli, this threshold can range from external forces such as blunt trauma to programmed processes such as apoptosis, autophagy, or necroptosis. This review focuses on apoptosis, which is one form of programmed cell death. It highlights the multiple signaling pathways that promote or inhibit apoptosis and reviews current clinical therapies that target apoptotic pathways in ovarian cancer.

Cell death in Porifera: molecular players in the game of apoptotic cell death in living fossils

2006 ◽  
Vol 84 (2) ◽  
pp. 307-321 ◽  
Author(s):  
M Wiens ◽  
W E.G Müller
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Apoptotic Cell ◽  
Molecular Signaling ◽  
Regeneration Capacity ◽  
The Past ◽  
Physiological Processes ◽  
Living Fossils ◽  
Core Components ◽  
Apoptotic Pathways

Apoptosis represents the morphological manifestation of programmed cell death and, paradoxically at first sight, it is a prerequisite for metazoan life. Thus, apoptosis is responsible for the demise of cells during many physiological processes. It is also accountable for the death of cells following exposure to countless stimuli. Therefore, it is obvious that apoptosis must be regulated by a complex network of various molecular signaling pathways. Research during the past 20 years has led to the identification of major functional groups of molecules involved in apoptotic pathways. These include members of the Bcl-2 superfamily, members of the TNF family, caspases, and their activators. Yet, the evolutionary conservation of those elements of the apoptotic machinery was only established from nematode to man. Sponges (phylum Porifera) are characterized by a remarkable regeneration capacity and longevity. Furthermore, they represent the phylogenetically oldest still extant metazoan taxon. Thus, research on these living fossils opens a window to the past, to the dawn of metazoan life. It allows us to trace the evolution of programmed cell death and its core components. This review summarizes the key findings and concepts which have emerged from studies of apoptosis in Porifera.

Sign in / Sign up

Export Citation Format

Share Document