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.

scholarly journals Production of Prodiginines Is Part of a Programmed Cell Death Process in Streptomyces coelicolor

2018 ◽  
Vol 9 ◽  
Author(s):  
Elodie Tenconi ◽  
Matthew F. Traxler ◽  
Charline Hoebreck ◽  
Gilles P. van Wezel ◽  
Sébastien Rigali
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Streptomyces Coelicolor ◽  
Death Process ◽  
Cell Death Process

scholarly journals Inflammation, necrosis, and the kinase RIP3 are key mediators of AAG-dependent alkylation-induced retinal degeneration

2019 ◽  
Vol 12 (568) ◽  
pp. eaau9216 ◽  
Author(s):  
Mariacarmela Allocca ◽  
Joshua J. Corrigan ◽  
Aprotim Mazumder ◽  
Kimberly R. Fake ◽  
Leona D. Samson
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Retinal Degeneration ◽  
Excision Repair ◽  
Alkylating Agents ◽  
Death Process ◽  
Partial Protection ◽  
Cell Death Process ◽  
Base Excision ◽  
Damage Marker

DNA-alkylating agents are commonly used to kill cancer cells, but the base excision repair (BER) pathway they trigger can also produce toxic intermediates that cause tissue damage, such as retinal degeneration (RD). Apoptosis, a process of programmed cell death, is assumed to be the main mechanism of this alkylation-induced photoreceptor (PR) cell death in RD. Here, we studied the involvement of necroptosis (another programmed cell death process) and inflammation in alkylation-induced RD. Male mice exposed to a methylating agent exhibited a reduced number of PR cell rows, active gliosis, and cytokine induction and macrophage infiltration in the retina. Dying PRs exhibited a necrotic morphology, increased 8-hydroxyguanosine abundance (an oxidative damage marker), and overexpression of the necroptosis-associated genes Rip1 and Rip3. The activity of PARP1, which mediates BER, cell death, and inflammation, was increased in PR cells and associated with the release of proinflammatory chemokine HMGB1 from PR nuclei. Mice lacking the anti-inflammatory cytokine IL-10 exhibited more severe RD, whereas deficiency of RIP3 (also known as RIPK3) conferred partial protection. Female mice were partially protected from alkylation-induced RD, showing reduced necroptosis and inflammation compared to males. PRs in mice lacking the BER-initiating DNA glycosylase AAG did not exhibit alkylation-induced necroptosis or inflammation. Our findings show that AAG-initiated BER at alkylated DNA bases induces sex-dependent RD primarily by triggering necroptosis and activating an inflammatory response that amplifies the original damage and, furthermore, reveal new potential targets to prevent this side effect of chemotherapy.

Programmed Cell Death (Apoptosis) and Cancer Chemotherapy

1996 ◽  
Vol 3 (4) ◽  
pp. 303-309 ◽  
Author(s):  
Samuel R. Denmeade ◽  
John T. Isaacs
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Morphological Changes ◽  
Malignant Cell ◽  
Death Process ◽  
Tumor Resistance ◽  
Apoptotic Pathway ◽  
Exogenous Agents ◽  
Specific Alteration ◽  
Energy Dependent

Background Programmed cell death involves a genetic reprogramming of the cell to promote an energy-dependent cascade of biochemical and morphological changes within the cell that result in its death and elimination. Methods The regulations and mechanisms of programmed cell death are reviewed with an emphasis on how derangement of this mechanism may be involved in modulating responsiveness to chemotherapy. Results Activation of this programmed death process is controlled by a series of endogenous cell-type-specific signals. In addition, a variety of exogenous cell-damaging treatments (eg, radiation, chemicals, and viruses) and most chemotherapeutic drugs can activate this pathway if sufficient injury to the cell occurs. Resistance to chemotherapy can involve alterations in the ability of a malignant cell to activate the programmed cell death (apoptotic) pathway when damaged by these exogenous agents. Conclusion The most important determinant of tumor resistance may be a generalized resistance to induction of programmed cell death rather than resistance based on specific alteration in drug/target interactions.

scholarly journals “Programmed Cell Death: A Process of Death for Survival” – How Far Terminology Pertinent for Cell Death in Unicellular Organisms

2018 ◽  
Vol 11 ◽  
pp. 117906601879025 ◽  
Author(s):  
Shiv Shanker Pandey ◽  
Samer Singh ◽  
Chandramani Pathak ◽  
Budhi Sagar Tiwari
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Normal Growth ◽  
Death Process ◽  
Target Cells ◽  
Dna Ladder ◽  
Cell Death Process ◽  
Unicellular Organisms ◽  
Multicellular Organisms ◽  
Dna Nicks

Programmed cell death (PCD) is genetically regulated phenomenon of selective elimination of target cells that are either under pathological conditions or unwanted for organism’s normal growth and development due to other reasons. The process although being genetically controlled is physiological in nature that renders some hallmarks like blebs in the cell membrane, lobe formation in nuclear membrane, DNA nicks resulting to DNA ladder of 200 bp, and downstream activation of caspases. Moreover, as the process refers to the death of “targeted cell”, the term is exclusively suitable for multicellular organisms. Number of reports advocate similar type of cell death process in unicellular organisms. As cell death in unicellular organisms is also reflected by the signature of PCD obtained in metazoans, such cell death has been grouped under the broad category of PCD. It is pertinent to mention that by definition a unicellular organism is made of a single cell wherein it carries out all of its life processes. Using the term “Programmed Cell Death” with a preset “survival strategy of the organism” for unicellular organisms looks misnomer. Therefore, this correspondence argues and requests recommendation committee on cell death to revisit for the nomenclature of the cell death process in the unicellular organisms.

scholarly journals Necrotic Death Pathway in FAS Receptor Signaling

2000 ◽  
Vol 151 (6) ◽  
pp. 1247-1256 ◽  
Author(s):  
Hirotaka Matsumura ◽  
Yusuke Shimizu ◽  
Yoshiyuki Ohsawa ◽  
Atsuo Kawahara ◽  
Yasuo Uchiyama ◽  
...  
Keyword(s):  
Cell Death ◽  
Cytochrome C ◽  
Fas Ligand ◽  
Morphological Changes ◽  
Death Receptor ◽  
Jurkat Cells ◽  
Death Process ◽  
Pyrrolidine Dithiocarbamate ◽  
Death Domain ◽  
Cell Death Process

A caspase 8–deficient subline (JB6) of human Jurkat cells can be killed by the oligomerization of Fas-associated protein with death domain (FADD). This cell death process is not accompanied by caspase activation, but by necrotic morphological changes. Here, we show that the death effector domain of FADD is responsible for the FADD-mediated necrotic pathway. This process was accompanied by a loss of mitochondrial transmembrane potential (ΔΨm), but not by the release of cytochrome c from mitochondria. Pyrrolidine dithiocarbamate, a metal chelator and antioxidant, efficiently inhibited the FADD-induced reduction of ΔΨm and necrotic cell death. When human Jurkat, or its transformants, expressing mouse Fas were treated with Fas ligand or anti–mouse Fas antibodies, the cells died, showing characteristics of apoptosis. A broad caspase inhibitor (z-VAD–fmk) blocked the apoptotic morphological changes and the release of cytochrome c. However, the cells still died, and this cell death process was accompanied by a strong reduction in ΔΨm, as well as necrotic morphological changes. The presence of z-VAD–fmk and pyrrolidine dithiocarbamate together blocked cell death, suggesting that both apoptotic and necrotic pathways can be activated through the Fas death receptor.

scholarly journals Acetic acid induces a programmed cell death process in the food spoilage yeast

2003 ◽  
Vol 3 (1) ◽  
pp. 91-96 ◽  
Author(s):  
P LUDOVICO ◽  
F SANSONETTY ◽  
M SILVA ◽  
M CORTEREAL
Keyword(s):  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Death Process ◽  
Food Spoilage ◽  
Spoilage Yeast ◽  
Cell Death Process

scholarly journals Exploring the Focal Role of Pyroptosis in Diabetes Mellitus

2021 ◽  
Vol 11 (5) ◽  
pp. 13557-13572
Keyword(s):  
Diabetes Mellitus ◽  
Cell Death ◽  
T Cell ◽  
Programmed Cell Death ◽  
Defense Mechanism ◽  
Death Process ◽  
Membrane Pores ◽  
Caspase 1 ◽  
Cell Death Process ◽  
Physiological Outcomes

Diabetes mellitus is a T cell-mediated disease associated with the depletion of beta cells responsible for insulin production. Although the disease is T cell-mediated, it undergoes various biochemical responses and programmed cell death. Programmed cell death, a distinct biochemical pathway in which cells die by eliciting various physiological outcomes. Pyroptosis, apoptosis, and necrosis are the three major forms of programmed cell death that function as a defense mechanism against various infections, diseases, and microorganisms. This review article focuses on the various pathological mechanisms of pyroptosis. Pyroptosis is distinguished by the caspase-1-dependent formation of plasma membrane pores, resulting in the release of pro-inflammatory cytokines, leading to cell lysis. Caspase-1, a protease which is an interleukin-1L-1β converting enzyme that initiates the cell death process by converting interleukin-1L-1β into mature inflammatory cytokine (mature form). Emerging evidence has made pyroptosis a vital trigger as well as an endogenic regulator of diabetes mellitus.

scholarly journals Jasmonic Acid and Ethylene Participate in the Gibberellin-Induced Ovule Programmed Cell Death Process in Seedless Pear ‘1913’ (Pyrus hybrid)

2021 ◽  
Vol 22 (18) ◽  
pp. 9844
Author(s):  
Huibin Wang ◽  
Shichao Zhang ◽  
Yingying Qu ◽  
Rui Gao ◽  
Yuxiong Xiao ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Jasmonic Acid ◽  
Regulatory Mechanism ◽  
Death Process ◽  
Strong Correlations ◽  
Ovule Abortion ◽  
Ethylene Precursor ◽  
Cell Death Process ◽  
Ja Signaling

Seedless fruit is a feature appreciated by consumers. The ovule abortion process is highly orchestrated and controlled by numerous environmental and endogenous signals. However, the mechanisms underlying ovule abortion in pear remain obscure. Here, we found that gibberellins (GAs) have diverse functions during ovules development between seedless pear ‘1913’ and seeded pear, and that GA4+7 activates a potential programmed cell death process in ‘1913’ ovules. After hormone analyses, strong correlations were determined among jasmonic acid (JA), ethylene and salicylic acid (SA) in seedless and seeded cultivars, and GA4+7 treatments altered the hormone accumulation levels in ovules, resulting in significant correlations between GA and both JA and ethylene. Additionally, SA contributed to ovule abortion in ‘1913’. Exogenously supplying JA, SA or the ethylene precursor 1-aminocyclopropane-1-carboxylic acid promoted ‘Bartlett’ seed death. The regulatory mechanism in which ethylene controls ovule death has been demonstrated; therefore, JA’s role in regulating ‘1913’ ovule abortion was investigated. A further study identified that the JA signaling receptor MYC2 bound the SENESCENCE-ASSOCIATED 39 promoter and triggered its expression to regulate ovule abortion. Thus, we established ovule abortion-related relationships between GA and the hormones JA, ethylene and SA, and we determined their synergistic functions in regulating ovule death.

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