scholarly journals Novel Nile Blue Analogue Stains Yeast Vacuolar Membrane, Endoplasmic Reticulum and Lipid Droplets, Inducing Cell Death through Vacuole Membrane Permeabilization

2021 ◽  
Vol 7 (11) ◽  
pp. 971
Author(s):  
João Carlos Canossa Ferreira ◽  
Carla Lopes ◽  
Ana Preto ◽  
Maria Sameiro Torres Gonçalves ◽  
Maria João Sousa
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Cell Biology ◽  
Lipid Droplets ◽  
Nile Blue ◽  
Vacuolar Membrane ◽  
Membrane Permeabilization ◽  
Death Process ◽  
Vacuole Membrane ◽  
Cell Death Process

Phenoxazine derivatives such as Nile Blue analogues are assumed to be increasingly relevant in cell biology due to their fluorescence staining capabilities and antifungal and anticancer activities. However, the mechanisms underlying their effects remain poorly elucidated. Using S. cerevisiae as a eukaryotic model, we found that BaP1, a novel 5- and 9-N-substituted benzo[a]phenoxazine synthesized in our laboratory, when used in low concentrations, accumulates and stains the vacuolar membrane and the endoplasmic reticulum. In contrast, at higher concentrations, BaP1 stains lipid droplets and induces a regulated cell death process mediated by vacuolar membrane permeabilization. BaP1 also induced mitochondrial fragmentation and depolarization but did not lead to ROS accumulation, changes in intracellular Ca2+, or loss of plasma membrane integrity. Additionally, our results show that the cell death process is dependent on the vacuolar protease Pep4p and that the vacuole permeabilization results in its translocation from the vacuole to the cytosol. In addition, although nucleic acids are commonly described as targets of benzo[a]phenoxazines, we did not find any alterations at the DNA level. Our observations highlight BaP1 as a promising molecule for pharmacological application, using vacuole membrane permeabilization as a targeted approach.

scholarly journals Correction: PML induces a novel caspase-independent cell death process

10.1038/8706 ◽  
1999 ◽  
Vol 22 (1) ◽  
pp. 115-115 ◽  
Author(s):  
Fredérique Quignon
Keyword(s):  
Cell Death ◽  
Death Process ◽  
Cell Death Process

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

Characterization of cell death process in plant cells induced by hipoxia and anoxia

2000 ◽  
Vol 28 (5) ◽  
pp. A372-A372
Author(s):  
E. N. Baranova ◽  
N. V. Kononenko ◽  
T. V. Bragina ◽  
G. M. Grineva ◽  
T. P. Astafurova ◽  
...  
Keyword(s):  
Cell Death ◽  
Plant Cells ◽  
Death Process ◽  
Cell Death Process

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 Oxidative Stress in Cell Death and Cardiovascular Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Tao Xu ◽  
Wei Ding ◽  
Xiaoyu Ji ◽  
Xiang Ao ◽  
Ying Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiovascular Diseases ◽  
Death Process ◽  
Ros Production ◽  
Disease Treatment ◽  
Physiological Conditions ◽  
Intracellular Ros ◽  
Cell Death Process ◽  
Molecular Components ◽  
Multiple Signaling

ROS functions as a second messenger and modulates multiple signaling pathways under the physiological conditions. However, excessive intracellular ROS causes damage to the molecular components of the cell, which promotes the pathogenesis of various human diseases. Cardiovascular diseases are serious threats to human health with extremely high rates of morbidity and mortality. Dysregulation of cell death promotes the pathogenesis of cardiovascular diseases and is the clinical target during the disease treatment. Numerous studies show that ROS production is closely linked to the cell death process and promotes the occurrence and development of the cardiovascular diseases. In this review, we summarize the regulation of intracellular ROS, the roles of ROS played in the development of cardiovascular diseases, and the programmed cell death induced by intracellular ROS. We also focus on anti-ROS system and the potential application of anti-ROS strategy in the treatment of cardiovascular diseases.

scholarly journals Research Resource: Monitoring Endoplasmic Reticulum Membrane Integrity in β-Cells at the Single-Cell Level

2015 ◽  
Vol 29 (3) ◽  
pp. 473-480 ◽  
Author(s):  
Kohsuke Kanekura ◽  
Jianhong Ou ◽  
Takashi Hara ◽  
Lihua J. Zhu ◽  
Fumihiko Urano
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Er Stress ◽  
Single Cell ◽  
Membrane Integrity ◽  
Membrane Permeabilization ◽  
Single Cell Level ◽  
Cell Level ◽  
Β Cell ◽  
Er Membrane

Abstract Endoplasmic reticulum (ER) membrane integrity is an emerging target for human chronic diseases associated with ER stress. Despite the underlying importance of compromised ER membrane integrity in disease states, the entire process leading to ER membrane permeabilization and cell death is still not clear due to technical limitations. Here we describe a novel method for monitoring ER membrane integrity at the single-cell level in real time. Using a β-cell line expressing ER-targeted redox sensitive green fluorescent protein, we could identify a β-cell population undergoing ER membrane permeabilization induced by palmitate and could monitor cell fate and ER stress of these cells at the single-cell level. Our method could be used to develop a novel therapeutic modality targeting the ER membrane for ER-associated disorders, including β-cell death in diabetes, neurodegeneration, and Wolfram syndrome.

scholarly journals Genome digestion is a dispensable consequence of physiological cell death mediated by cytotoxic T lymphocytes.

1992 ◽  
Vol 12 (7) ◽  
pp. 3060-3069 ◽  
Author(s):  
D S Ucker ◽  
P S Obermiller ◽  
W Eckhart ◽  
J R Apgar ◽  
N A Berger ◽  
...  
Keyword(s):  
Cell Death ◽  
Cytotoxic T Lymphocyte ◽  
Death Process ◽  
Cell Nuclei ◽  
Calcium Dependent ◽  
Nuclear Envelope Breakdown ◽  
Murine Fibroblast ◽  
Cell Death Process ◽  
Cell Suicide ◽  
Physiological Cell Death

We examined virally transformed murine fibroblast clones as targets for cytotoxic T lymphocyte (CTL)-triggered lysis and genome digestion. Strikingly, while all clones were essentially equivalent in the ability to be lysed, one clone, SV3T3-B2.1, failed to exhibit genome digestion associated with CTL attack. Other aspects of the physiological cell death process, including loss of adhesion and nuclear envelope breakdown (lamin phosphorylation and solubilization), were not altered in this clone. The absence of genome digestion associated with CTL-induced cell death correlated with the absence of endodeoxyribonuclease activity in the nuclei of that clone. Characterization of the activity affected identifies a calcium-dependent, DNase I-like endonuclease of approximately 40 kDa, normally present constitutively in all cell nuclei, as the enzyme responsible for genome digestion associated with CTL-mediated cell death. These observations indicate that neither genome digestion per se nor its consequences [such as activation of poly(ADP-ribose) polymerase] are essential for cell death resulting from the triggering of this cell suicide process.

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