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
Citations
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Autophagy inhibition of hsa-miR-19a-3p/19b-3p by targeting TGF-β R II during TGF-β1-induced fibrogenesis in human cardiac fibroblasts
Meijuan Zou,Fang Wang,Rui Gao,Wu Jingjing,Yingwei Ou,Xuguan Chen,Tongshan Wang,Xin Zhou,Wei Zhu,Ping Li,Lian-Wen Qi,Ting Jiang,Weiwei Wang,Chunyu Li,Jun Chen,He Qifang,Yan Chen +16 more
TL;DR: This study uncovers a novel mechanism that miR-19a-3p/19b-3P inhibits autophagy-mediated fibrogenesis by targeting TGF-β R II.
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Methamphetamine induces autophagy as a pro-survival response against apoptotic endothelial cell death through the Kappa opioid receptor
TL;DR: It is reported here that while chronic exposure to METH disrupts barrier function of primary human brain microvascular endothelial cells (HBMECs), an early pro-survival response is observed following acute exposure by induction of autophagic mechanisms, and kappa opioid receptor can be therapeutically exploited for attenuating METH-induced BBB dysfunction.
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Targeting LC3 and Beclin-1 autophagy genes suppresses proliferation, survival, migration and invasion by inhibition of Cyclin-D1 and uPAR/Integrin β1/ Src signaling in triple negative breast cancer cells
Zuhal Hamurcu,Nesrin Delibaşı,Seda Geçene,Elif Funda Sener,Hamiyet Donmez-Altuntas,Yusuf Ozkul,Halit Canatan,Bulent Ozpolat +7 more
TL;DR: It is suggested that LC3 and Beclin-1 are required for cell proliferation, survival, migration and invasion, and may contribute to tumor growth and progression of highly aggressive and metastatic TNBC cells and therapeutic targeting of autophagy genes may be a potential therapeutic strategy for TNBC in breast cancer.
Journal ArticleDOI
Induction of oxiapoptophagy on 158N murine oligodendrocytes treated by 7-ketocholesterol-, 7β-hydroxycholesterol-, or 24(S)-hydroxycholesterol: Protective effects of α-tocopherol and docosahexaenoic acid (DHA; C22:6 n-3).
Thomas Nury,Amira Zarrouk,John J. Mackrill,Mohammad Samadi,Philippe Durand,Jean-Marc Riedinger,Margaux Doria,Anne Vejux,Emeric Limagne,Dominique Delmas,Michel Prost,Thibault Moreau,Mohamed Hammami,Régis Delage-Mourroux,Nora M. O'Brien,Gérard Lizard +15 more
TL;DR: In 158N murine oligodendrocytes, the concept that oxiapoptophagy, which can be inhibited by VitE and DHA, could be a particular mode of cell death elicited by cytotoxic oxysterols is supported.
Journal ArticleDOI
CHOP mediates ASPP2-induced autophagic apoptosis in hepatoma cells by releasing Beclin-1 from Bcl-2 and inducing nuclear translocation of Bcl-2
Kai Liu,Ying Shi,Xianghua Guo,Shuyan Wang,Yabo Ouyang,Meijun Hao,Daojie Liu,Luxin Qiao,Ning Li,Jiasheng Zheng,De-Xi Chen +10 more
TL;DR: The results show that ASPP2 induces the expression of damage-regulated autophagy modulator (DRAM), another critical factor that cooperates with free Beclin-1 to induce autophagic apoptosis and open a new avenue for promotingAutophagy in treatments to cure hepatocellular carcinoma.
References
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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
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Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation
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Journal ArticleDOI
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.
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Mitochondrial Membrane Permeabilization in Cell Death
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