Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes
Lorenzo Galluzzi,Lorenzo Galluzzi,Lorenzo Galluzzi,Stuart A. Aaronson,John M. Abrams,Emad S. Alnemri,David W. Andrews,Eric H. Baehrecke,Nicolas G. Bazan,Mikhail V. Blagosklonny,Klas Blomgren,Klas Blomgren,Christoph Borner,Dale E. Bredesen,Dale E. Bredesen,Catherine Brenner,Maria Castedo,Maria Castedo,Maria Castedo,John A. Cidlowski,Aaron Ciechanover,Gerald M. Cohen,V De Laurenzi,R De Maria,Mohanish Deshmukh,Brian David Dynlacht,Wafik S. El-Deiry,Richard A. Flavell,Richard A. Flavell,Simone Fulda,Carmen Garrido,Carmen Garrido,Pierre Golstein,Pierre Golstein,Pierre Golstein,Marie-Lise Gougeon,Douglas R. Green,Hinrich Gronemeyer,Hinrich Gronemeyer,Hinrich Gronemeyer,György Hajnóczky,J. M. Hardwick,Michael O. Hengartner,Hidenori Ichijo,Marja Jäättelä,Oliver Kepp,Oliver Kepp,Oliver Kepp,Adi Kimchi,Daniel J. Klionsky,Richard A. Knight,Sally Kornbluth,Sharad Kumar,Beth Levine,Beth Levine,Stuart A. Lipton,Enrico Lugli,Frank Madeo,Walter Malorni,Jean-Christophe Marine,Seamus J. Martin,Jan Paul Medema,Patrick Mehlen,Patrick Mehlen,Gerry Melino,Gerry Melino,Ute M. Moll,Ute M. Moll,Eugenia Morselli,Eugenia Morselli,Eugenia Morselli,Shigekazu Nagata,Donald W. Nicholson,Pierluigi Nicotera,Gabriel Núñez,Moshe Oren,Josef M. Penninger,Shazib Pervaiz,Marcus E. Peter,Mauro Piacentini,Jochen H. M. Prehn,Hamsa Puthalakath,Gabriel A. Rabinovich,Rosario Rizzuto,Cecília M. P. Rodrigues,David C. Rubinsztein,Thomas Rudel,Luca Scorrano,Hans-Uwe Simon,Hermann Steller,Hermann Steller,J. Tschopp,Yoshihide Tsujimoto,Peter Vandenabeele,Ilio Vitale,Ilio Vitale,Ilio Vitale,Karen H. Vousden,Richard J. Youle,Junying Yuan,Boris Zhivotovsky,Guido Kroemer,Guido Kroemer,Guido Kroemer +103 more
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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 cellsread more
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Malathion increases apoptotic cell death by inducing lysosomal membrane permeabilization in N2a neuroblastoma cells: a model for neurodegeneration in Alzheimer’s disease
TL;DR: The data suggest that the non-cholinergic effect of malathion may be mediated by apoptotic cell death via LMP induction in N2a cells.
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Mitochondrion-Specific Blinking Fluorescent Bioprobe for Nanoscopic Monitoring of Mitophagy.
TL;DR: A fluorescent carbon dot, which can selectively target mitochondria in live cell (named as MitoCD), which can effectively accumulate in mitochondria regardless of the decrease or vanishing of mitochondrial membrane potential (MMP), enabling the exploration of MMP-independent mitochondrial process.
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Melatonin modulates autophagy and inflammation protecting human placental trophoblast from hypoxia/reoxygenation
Lucas Sagrillo-Fagundes,Lucas Sagrillo-Fagundes,Eugania Maria Assuncao Salustiano,Rodrigo Ruano,Regina P. Markus,Cathy Vaillancourt,Cathy Vaillancourt +6 more
TL;DR: It is suggested that H/R, which is present in pregnancy complications, inhibits endogenous melatonin production, thereby contributing to reduced syncytiotrophoblast viability and contributing to improved fetal outcomes.
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Altered autophagic flux enhances inflammatory responses during inflammation-induced preterm labor
Varkha Agrawal,Mukesh K. Jaiswal,Timothy M. Mallers,Gajendra K. Katara,Alice Gilman-Sachs,Kenneth D. Beaman,Emmet Hirsch +6 more
TL;DR: It is demonstrated that the autophagy related genes Atg4c and Atg7 decrease significantly in uterus and placenta during IPTL but not NIPTL, the first evidence of an association between altered autophagic flux and hyper-inflammation and labor in IPTL.
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Nicotinate-Curcumin Impedes Foam Cell Formation from THP-1 Cells through Restoring Autophagy Flux
Hong-Feng Gu,Hai-Zhe Li,Ya-Ling Tang,Xiao-Qing Tang,Xi-Long Zheng,Xi-Long Zheng,Duan-Fang Liao +6 more
TL;DR: The findings suggest that NC decreases lipid accumulation in THP-1 cells through restoring autophagy flux, and implicate that NC may be a potential therapeutic reagent to reverse atherosclerosis.
References
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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.
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Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation
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Molecular characterization of mitochondrial apoptosis-inducing factor
Santos A. Susin,Hans K. Lorenzo,Naoufal Zamzami,Isabel Marzo,Bryan E. Snow,Joan Mangion,Etienne Jacotot,Paola Costantini,Markus Loeffler,Nathanael Larochette,David R. Goodlett,Ruedi Aebersold,David P. Siderovski,Josef M. Penninger,Guido Kroemer +14 more
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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