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
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 drives osteogenic differentiation of human gingival mesenchymal stem cells.
Chiara Vidoni,Alessandra Ferraresi,Eleonora Secomandi,Letizia Vallino,Chiara Gardin,Barbara Zavan,Carmen Mortellaro,Ciro Isidoro +7 more
TL;DR: It is shown that HGMSCs can differentiate into osteoblasts when cultured in the presence of appropriate factors and that resveratrol accelerates this process by up-regulating autophagy.
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Hepatitis B Virus Induces Autophagy to Promote its Replication by the Axis of miR-192-3p-XIAP Through NF kappa B Signaling
Jingwen Wang,Jianwen Chen,Yang Liu,Xianhuang Zeng,Mingcong Wei,Shaoshuai Wu,Qiushuang Xiong,Feifei Song,Xu Yuan,Yu Xiao,Yun Cao,Changyong Li,Lang Chen,Mingxiong Guo,Yun-Bo Shi,Guihong Sun,Deyin Guo +16 more
TL;DR: Wang et al. as discussed by the authors showed that decreasing levels of the expression of the miRNA miR-192-3p is associated with rising levels of hepatitis B virus DNA in the serum of HBV patients.
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Upregulation of SQSTM1/p62 contributes to nickel-induced malignant transformation of human bronchial epithelial cells
Haishan Huang,Junlan Zhu,Yang Li,Liping Zhang,Jiayan Gu,Qipeng Xie,Honglei Jin,Xun Che,Jingxia Li,Chao Huang,Lung Chi Chen,Jianxin Lyu,Jimin Gao,Chuanshu Huang +13 more
TL;DR: A novel SQSTM1 regulatory network is demonstrated that promotes a nickel-induced tumorigenic effect in human bronchial epithelial cells, which is negatively controlled by an autophagic cascade following nickel exposure.
Journal ArticleDOI
The Quantitative-Phase Dynamics of Apoptosis and Lytic Cell Death
TL;DR: Time-dependent changes in quantitative phase-based parameters during cell death were determined and methodology useable for rapid and label-free assessment of direct cell death was introduced, distinction between apoptosis and primary lytic cell death based on morphologic features was made.
Journal ArticleDOI
Inhibition of autophagy increased AGE/ROS-mediated apoptosis in mesangial cells
TL;DR: The data suggest that ROS were the mediators of AGE-induced mesangial cell apoptosis and that autophagy was likely to be the mechanism that was triggered to repair the ROS-induced damage in the A GE-treated cells and thereby promote cell survival.
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.
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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.
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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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