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Open AccessJournal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes

Lorenzo Galluzzi, +103 more
- 17 Apr 2009 - 
- Vol. 16, Iss: 8, pp 1093-1107
TLDR
A nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls is provided and the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells is emphasized.
Abstract
Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios Thus far, dozens of methods have been proposed to quantify cell death-related parameters However, no guidelines exist regarding their use and interpretation, and nobody has thoroughly annotated the experimental settings for which each of these techniques is most appropriate Here, we provide a nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls These guidelines are intended for investigators who study cell death, as well as for reviewers who need to constructively critique scientific reports that deal with cellular demise Given the difficulties in determining the exact number of cells that have passed the point-of-no-return of the signaling cascades leading to cell death, we emphasize the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells

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Nox1 causes ileocolitis in mice deficient in glutathione peroxidase-1 and -2.

TL;DR: The male TKO and female het-TKO mice have nearly no signs of disease and are virtually disease-free when monitored from 8 through 50 days of age, and it is proposed that ileocolitis in the DKO mice is caused by Nox1, which is induced by TNF.
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IP3 accumulation and/or inositol depletion: two downstream lithium's effects that may mediate its behavioral and cellular changes.

TL;DR: Lithium affects the phosphatidylinositol signaling system in two ways: depleting inositol, consequently decreasing phosphoinositides; elevating inositl monophosphate levels followed by phosphoinotides accumulation; each or both may mediate lithium-induced behavior.
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Aptamer-based bio-barcode assay for the detection of cytochrome-c released from apoptotic cells

TL;DR: A 76-mer monoclonal aptamer against cytochrome-c (cyto-c) and this single-stranded DNA in defined 3D structure for cy to-c was used in the BBC assay for both recognition and readout reporting and was sensitive enough to detect the cyto- c in culture medium released from the apoptotic cells after drug treatment at the picomolar level.
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Bromelain inhibits the ability of colorectal cancer cells to proliferate via activation of ROS production and autophagy.

TL;DR: Bromelain inhibited CRC cell growth in cell lines and tumor growth in the zebrafish and xenograft mouse models and can offer a cheap alternative to current therapies.
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Computational model for autophagic vesicle dynamics in single cells

TL;DR: The development of a computational model describing autophagic vesicle dynamics in a mammalian system is presented and can serve as the foundation for future efforts aimed at quantitative characterization of autophagy.
References
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Journal ArticleDOI

Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation.

TL;DR: The extent of tissue-PCD revealed by this method is considerably greater than apoptosis detected by nuclear morphology, and thus opens the way for a variety of studies.
Journal ArticleDOI

The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of Apoptosis

TL;DR: In a cell-free apoptosis system, mitochondria spontaneously released cytochrome c, which activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology, and Bcl-2 acts to inhibit cy tochrome c translocation, thereby blocking caspase activation and the apoptotic process.
Journal ArticleDOI

Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation

A. H. Wyllie
- 10 Apr 1980 - 
TL;DR: It is shown here that this morphological change is closely associated with excision of nucleosome chains from nuclear chromatin, apparently through activation of an intracellular, but non-lysosomal, endonuclease.
Journal ArticleDOI

Molecular characterization of mitochondrial apoptosis-inducing factor

TL;DR: The identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei is reported, indicating that AIF is a mitochondrial effector of apoptotic cell death.
Journal ArticleDOI

Mitochondrial Membrane Permeabilization in Cell Death

TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
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