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27. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, Dieter, Agostinis, Patrizia, Alnemri, E. S., Altucci, Lucia, Amelio, Ivano, Andrews, D. W., Annicchiarico-Petruzzelli, Margherita, Antonov, A. V., Arama, Eli, Baehrecke, E. H., Barlev, N. A., Bazan, N. G., Bernassola, Francesca, Bertrand, M. J. M., Bianchi, Katiuscia, Blagosklonny, M. V., Blomgren, Kla, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, F. K. -M., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, Aaron, Cohen, G. M., Conrad, Marcu, Cubillos-Ruiz, J. R., Czabotar, P. E., D’Angiolella, Vincenzo, Dawson, T. M., Dawson, V. L., de Laurenzi, Vincenzo, De Maria Marchiano, Ruggero, Debatin, Klaus-Michael, Deberardinis, R. J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, V. M., Dixon, S. J., Duckett, C. S., Dynlacht, B. D., El-Deiry, W. S., Elrod, J. W., Fimia, Gian Maria, Fulda, Simone, García-Sáez, A. J., Garg, A. D., Garrido, Carmen, Gavathiotis, Evripidi, Golstein, Pierre, Gottlieb, Eyal, Green, D. R., Greene, L. A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. M., Harris, I. S., Hengartner, M. O., Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, P. J., Juin, P. P., Kaiser, W. J., Karin, Michael, Kaufmann, Thoma, Kepp, Oliver, Kimchi, Adi, Kitsis, R. N., Klionsky, D. J., Knight, R. A., Kumar, Sharad, Lee, S. W., Lemasters, J. J., Levine, Beth, Linkermann, Andrea, Lipton, S. A., Lockshin, R. A., López-Otín, Carlo, Lowe, S. W., Luedde, Tom, Lugli, Enrico, Macfarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, S. J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, E. A., Molkentin, J. D., Moll, U. M., Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theochari, Pasparakis, Manoli, Penninger, J. M., Pereira, D. M., Pervaiz, Shazib, Peter, M. E., Piacentini, Mauro, Pinton, Paolo, Prehn, J. H. M., Puthalakath, Hamsa, Rabinovich, G. A., Rehm, Marku, Rizzuto, Rosario, Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, Thoma, Ryan, K. M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, B. R., Strasser, Andrea, Szabadkai, Gyorgy, Tait, S. W. G., Tang, Daolin, Tavernarakis, Nektario, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Bori, Vanden Berghe, Tom, Vandenabeele, Peter, Vander Heiden, M. G., Villunger, Andrea, Virgin, H. W., Vousden, K. H., Vucic, Domagoj, Wagner, E. F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, J. A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Bori, Zitvogel, Laurence, Melino, Gerry, Kroemer, Guido, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), Sistigu, Antonella (ORCID:0000-0002-2528-1238), Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, Dieter, Agostinis, Patrizia, Alnemri, E. S., Altucci, Lucia, Amelio, Ivano, Andrews, D. W., Annicchiarico-Petruzzelli, Margherita, Antonov, A. V., Arama, Eli, Baehrecke, E. H., Barlev, N. A., Bazan, N. G., Bernassola, Francesca, Bertrand, M. J. M., Bianchi, Katiuscia, Blagosklonny, M. V., Blomgren, Kla, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, F. K. -M., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, Aaron, Cohen, G. M., Conrad, Marcu, Cubillos-Ruiz, J. R., Czabotar, P. E., D’Angiolella, Vincenzo, Dawson, T. M., Dawson, V. L., de Laurenzi, Vincenzo, De Maria Marchiano, Ruggero, Debatin, Klaus-Michael, Deberardinis, R. J., Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, V. M., Dixon, S. J., Duckett, C. S., Dynlacht, B. D., El-Deiry, W. S., Elrod, J. W., Fimia, Gian Maria, Fulda, Simone, García-Sáez, A. J., Garg, A. D., Garrido, Carmen, Gavathiotis, Evripidi, Golstein, Pierre, Gottlieb, Eyal, Green, D. R., Greene, L. A., Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J. M., Harris, I. S., Hengartner, M. O., Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, P. J., Juin, P. P., Kaiser, W. J., Karin, Michael, Kaufmann, Thoma, Kepp, Oliver, Kimchi, Adi, Kitsis, R. N., Klionsky, D. J., Knight, R. A., Kumar, Sharad, Lee, S. W., Lemasters, J. J., Levine, Beth, Linkermann, Andrea, Lipton, S. A., Lockshin, R. A., López-Otín, Carlo, Lowe, S. W., Luedde, Tom, Lugli, Enrico, Macfarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, Manic, Gwenola, Marine, Jean-Christophe, Martin, S. J., Martinou, Jean-Claude, Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Sonia, Miao, E. A., Molkentin, J. D., Moll, U. M., Muñoz-Pinedo, Cristina, Nagata, Shigekazu, Nuñez, Gabriel, Oberst, Andrew, Oren, Moshe, Overholtzer, Michael, Pagano, Michele, Panaretakis, Theochari, Pasparakis, Manoli, Penninger, J. M., Pereira, D. M., Pervaiz, Shazib, Peter, M. E., Piacentini, Mauro, Pinton, Paolo, Prehn, J. H. M., Puthalakath, Hamsa, Rabinovich, G. A., Rehm, Marku, Rizzuto, Rosario, Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, Thoma, Ryan, K. M., Sayan, Emre, Scorrano, Luca, Shao, Feng, Shi, Yufang, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stockwell, B. R., Strasser, Andrea, Szabadkai, Gyorgy, Tait, S. W. G., Tang, Daolin, Tavernarakis, Nektario, Thorburn, Andrew, Tsujimoto, Yoshihide, Turk, Bori, Vanden Berghe, Tom, Vandenabeele, Peter, Vander Heiden, M. G., Villunger, Andrea, Virgin, H. W., Vousden, K. H., Vucic, Domagoj, Wagner, E. F., Walczak, Henning, Wallach, David, Wang, Ying, Wells, J. A., Wood, Will, Yuan, Junying, Zakeri, Zahra, Zhivotovsky, Bori, Zitvogel, Laurence, Melino, Gerry, Kroemer, Guido, De Maria Marchiano, Ruggero (ORCID:0000-0003-2255-0583), and Sistigu, Antonella (ORCID:0000-0002-2528-1238)

Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018

35. Essential versus accessory aspects of cell death: Recommendations of the NCCD 2015

Author

Galluzzi, L., Bravo-San Pedro, J. M., Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, D., Alnemri, E. S., Altucci, L., Andrews, D., Annicchiarico-Petruzzelli, M., Baehrecke, E. H., Bazan, N. G., Bertrand, M. J., Bianchi, K., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Campanella, M., Candi, E., Cecconi, F., Chan, F. K., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, A., Dawson, T. M., Dawson, V. L., De Laurenzi, V., De Maria Marchiano, Ruggero, Debatin, K. -M., Di Daniele, N., Dixit, V. M., Dynlacht, B. D., El-Deiry, W. S., Fimia, G. M., Flavell, R. A., Fulda, S., Garrido, C., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnoczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Joseph, B., Jost, P. J., Kaufmann, T., Kepp, O., Klionsky, D. J., Knight, R. A., Kumar, S., Lemasters, J. J., Levine, B., Linkermann, A., Lipton, S. A., Lockshin, R. A., López-Otín, C., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C., Martin, S. J., Martinou, J. -C., Medema, Jan Paul, Meier, P., Melino, S., Mizushima, N., Moll, U., Muñoz-Pinedo, C., Nuñez, G., Oberst, A., Panaretakis, T., Penninger, J. M., Peter, M. E., Piacentini, M., Calzavara Pinton, Piergiacomo, Prehn, J. H., Puthalakath, H., Rabinovich, G. A., Ravichandran, K. S., Rizzuto, R., Rodrigues, C. M., Rubinsztein, D. C., Rudel, T., Shi, Y., Simon, H. -U., Stockwell, B. R., Szabadkai, G., Tait, S. W., Tang, H. L., Tavernarakis, N., Tsujimoto, Y., Vanden Berghe, T., Vandenabeele, P., Villunger, A., Wagner, E. F., Walczak, H., White, E., Wood, W. G., Yuan, J., Zakeri, Z., Zhivotovsky, B., Melino, G., Kroemer, G., Vitale, I., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., Calzavara Pinton, P., Galluzzi, L., Bravo-San Pedro, J. M., Vitale, Ilio, Aaronson, S. A., Abrams, J. M., Adam, D., Alnemri, E. S., Altucci, L., Andrews, D., Annicchiarico-Petruzzelli, M., Baehrecke, E. H., Bazan, N. G., Bertrand, M. J., Bianchi, K., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Campanella, M., Candi, E., Cecconi, F., Chan, F. K., Chandel, N. S., Cheng, E. H., Chipuk, J. E., Cidlowski, J. A., Ciechanover, A., Dawson, T. M., Dawson, V. L., De Laurenzi, V., De Maria Marchiano, Ruggero, Debatin, K. -M., Di Daniele, N., Dixit, V. M., Dynlacht, B. D., El-Deiry, W. S., Fimia, G. M., Flavell, R. A., Fulda, S., Garrido, C., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnoczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Joseph, B., Jost, P. J., Kaufmann, T., Kepp, O., Klionsky, D. J., Knight, R. A., Kumar, S., Lemasters, J. J., Levine, B., Linkermann, A., Lipton, S. A., Lockshin, R. A., López-Otín, C., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C., Martin, S. J., Martinou, J. -C., Medema, Jan Paul, Meier, P., Melino, S., Mizushima, N., Moll, U., Muñoz-Pinedo, C., Nuñez, G., Oberst, A., Panaretakis, T., Penninger, J. M., Peter, M. E., Piacentini, M., Calzavara Pinton, Piergiacomo, Prehn, J. H., Puthalakath, H., Rabinovich, G. A., Ravichandran, K. S., Rizzuto, R., Rodrigues, C. M., Rubinsztein, D. C., Rudel, T., Shi, Y., Simon, H. -U., Stockwell, B. R., Szabadkai, G., Tait, S. W., Tang, H. L., Tavernarakis, N., Tsujimoto, Y., Vanden Berghe, T., Vandenabeele, P., Villunger, A., Wagner, E. F., Walczak, H., White, E., Wood, W. G., Yuan, J., Zakeri, Z., Zhivotovsky, B., Melino, G., Kroemer, G., Vitale, I., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., and Calzavara Pinton, P.

Abstract

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.

Published
2015

38. Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Author

Galluzzi, L, primary, Bravo-San Pedro, J M, additional, Vitale, I, additional, Aaronson, S A, additional, Abrams, J M, additional, Adam, D, additional, Alnemri, E S, additional, Altucci, L, additional, Andrews, D, additional, Annicchiarico-Petruzzelli, M, additional, Baehrecke, E H, additional, Bazan, N G, additional, Bertrand, M J, additional, Bianchi, K, additional, Blagosklonny, M V, additional, Blomgren, K, additional, Borner, C, additional, Bredesen, D E, additional, Brenner, C, additional, Campanella, M, additional, Candi, E, additional, Cecconi, F, additional, Chan, F K, additional, Chandel, N S, additional, Cheng, E H, additional, Chipuk, J E, additional, Cidlowski, J A, additional, Ciechanover, A, additional, Dawson, T M, additional, Dawson, V L, additional, De Laurenzi, V, additional, De Maria, R, additional, Debatin, K-M, additional, Di Daniele, N, additional, Dixit, V M, additional, Dynlacht, B D, additional, El-Deiry, W S, additional, Fimia, G M, additional, Flavell, R A, additional, Fulda, S, additional, Garrido, C, additional, Gougeon, M-L, additional, Green, D R, additional, Gronemeyer, H, additional, Hajnoczky, G, additional, Hardwick, J M, additional, Hengartner, M O, additional, Ichijo, H, additional, Joseph, B, additional, Jost, P J, additional, Kaufmann, T, additional, Kepp, O, additional, Klionsky, D J, additional, Knight, R A, additional, Kumar, S, additional, Lemasters, J J, additional, Levine, B, additional, Linkermann, A, additional, Lipton, S A, additional, Lockshin, R A, additional, López-Otín, C, additional, Lugli, E, additional, Madeo, F, additional, Malorni, W, additional, Marine, J-C, additional, Martin, S J, additional, Martinou, J-C, additional, Medema, J P, additional, Meier, P, additional, Melino, S, additional, Mizushima, N, additional, Moll, U, additional, Muñoz-Pinedo, C, additional, Nuñez, G, additional, Oberst, A, additional, Panaretakis, T, additional, Penninger, J M, additional, Peter, M E, additional, Piacentini, M, additional, Pinton, P, additional, Prehn, J H, additional, Puthalakath, H, additional, Rabinovich, G A, additional, Ravichandran, K S, additional, Rizzuto, R, additional, Rodrigues, C M, additional, Rubinsztein, D C, additional, Rudel, T, additional, Shi, Y, additional, Simon, H-U, additional, Stockwell, B R, additional, Szabadkai, G, additional, Tait, S W, additional, Tang, H L, additional, Tavernarakis, N, additional, Tsujimoto, Y, additional, Vanden Berghe, T, additional, Vandenabeele, P, additional, Villunger, A, additional, Wagner, E F, additional, Walczak, H, additional, White, E, additional, Wood, W G, additional, Yuan, J, additional, Zakeri, Z, additional, Zhivotovsky, B, additional, Melino, G, additional, and Kroemer, G, additional

Published
2014
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40. Calcium-independent phospholipase A2 regulates retinal pigment epithelium proliferation and may be important in the pathogenesis of retinal diseases

Author

Kolko, M, Kiilgaard, J F, Wang, J, Poulsen, K A, Andreasen, J R, la Cour, M, Nissen, M H, Heegaard, S, Bazan, N G, Prause, J U, Kolko, M, Kiilgaard, J F, Wang, J, Poulsen, K A, Andreasen, J R, la Cour, M, Nissen, M H, Heegaard, S, Bazan, N G, and Prause, J U

Abstract

Udgivelsesdato: 2009-Sep, Calcium-independent phospholipase A2, group VIA (iPLA2-VIA) is involved in cell proliferation. This study aimed to evaluate the role of iPLA2-VIA in retinal pigment epithelium (RPE) cell proliferation and in retinal diseases involving RPE proliferation. A human RPE cell line (ARPE-19) was used to explore this role in vitro. Proliferating ARPE-19 cells had increased expression and activity of iPLA2-VIA. iPLA2-VIA was found in the nuclei of proliferating ARPE-19 cells, whereas in confluent ARPE-19 cells, with limited proliferation, iPLA2-VIA was primarily found in the cytosol. Inhibition of iPLA2-VIA decreased the rate of proliferation, whereas over expression of iPLA2-VIA increased the rate of proliferation. Using an experimental porcine model of RPE proliferation we demonstrated significant nuclear upregulation of iPLA2-VIA in proliferating RPE cells in vivo. We furthermore evaluated the expression of iPLA2-VIA in proliferative vitreoretinopathy (PVR). PVR membranes revealed nuclear expression of iPLA2-VIA in the RPE cells which had migrated and participated in the formation of the membranes. Overall, the present results point to an important role of iPLA2-VIA in the regulation of RPE proliferation suggesting that iPLA2-VIA may be considered as a possible pharmaceutical target in retinal diseases involving RPE proliferation and migration.

Published
2009

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

Author

Galluzzi, L., Aaronson, S. A., Abrams, J., Alnemri, E. S., Andrews, D. W., Baehrecke, E. H., Bazan, N. G., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Castedo, M., Cidlowski, J. A., Ciechanover, A., Cohen, G. M., De Laurenzi, V., De Maria Marchiano, Ruggero, Deshmukh, M., Dynlacht, B. D., El-Deiry, W. S., Flavell, R. A., Fulda, S., Garrido, C., Golstein, P., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnóczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Jäättelä, M., Kepp, O., Kimchi, A., Klionsky, D. J., Knight, R. A., Kornbluth, S., Kumar, S., Levine, B., Lipton, S. A., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C. W., Martin, S. J., Medema, Jan Paul, Mehlen, P., Melino, G., Moll, U. M., Morselli, E., Nagata, S., Nicholson, D. W., Nicotera, P., Nuñez, G., Oren, M., Penninger, J., Pervaiz, S., Peter, M. E., Piacentini, M., Prehn, J. H. M., Puthalakath, H., Rabinovich, G. A., Rizzuto, R., Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, T., Scorrano, L., Simon, H. -U., Steller, H., Tschopp, J., Tsujimoto, Y., Vandenabeele, P., Vitale, Ilio, Vousden, K. H., Youle, R. J., Yuan, J., Zhivotovsky, B., Kroemer, G., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., Vitale, I., Galluzzi, L., Aaronson, S. A., Abrams, J., Alnemri, E. S., Andrews, D. W., Baehrecke, E. H., Bazan, N. G., Blagosklonny, M. V., Blomgren, K., Borner, C., Bredesen, D. E., Brenner, C., Castedo, M., Cidlowski, J. A., Ciechanover, A., Cohen, G. M., De Laurenzi, V., De Maria Marchiano, Ruggero, Deshmukh, M., Dynlacht, B. D., El-Deiry, W. S., Flavell, R. A., Fulda, S., Garrido, C., Golstein, P., Gougeon, M. -L., Green, D. R., Gronemeyer, H., Hajnóczky, G., Hardwick, J. M., Hengartner, M. O., Ichijo, H., Jäättelä, M., Kepp, O., Kimchi, A., Klionsky, D. J., Knight, R. A., Kornbluth, S., Kumar, S., Levine, B., Lipton, S. A., Lugli, E., Madeo, F., Malorni, W., Marine, J. -C. W., Martin, S. J., Medema, Jan Paul, Mehlen, P., Melino, G., Moll, U. M., Morselli, E., Nagata, S., Nicholson, D. W., Nicotera, P., Nuñez, G., Oren, M., Penninger, J., Pervaiz, S., Peter, M. E., Piacentini, M., Prehn, J. H. M., Puthalakath, H., Rabinovich, G. A., Rizzuto, R., Rodrigues, C. M. P., Rubinsztein, D. C., Rudel, T., Scorrano, L., Simon, H. -U., Steller, H., Tschopp, J., Tsujimoto, Y., Vandenabeele, P., Vitale, Ilio, Vousden, K. H., Youle, R. J., Yuan, J., Zhivotovsky, B., Kroemer, G., De Maria Marchiano, R. (ORCID:0000-0003-2255-0583), Medema, J. P., and Vitale, I.

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.

Published
2009

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

Author

Galluzzi, L, primary, Aaronson, S A, additional, Abrams, J, additional, Alnemri, E S, additional, Andrews, D W, additional, Baehrecke, E H, additional, Bazan, N G, additional, Blagosklonny, M V, additional, Blomgren, K, additional, Borner, C, additional, Bredesen, D E, additional, Brenner, C, additional, Castedo, M, additional, Cidlowski, J A, additional, Ciechanover, A, additional, Cohen, G M, additional, De Laurenzi, V, additional, De Maria, R, additional, Deshmukh, M, additional, Dynlacht, B D, additional, El-Deiry, W S, additional, Flavell, R A, additional, Fulda, S, additional, Garrido, C, additional, Golstein, P, additional, Gougeon, M-L, additional, Green, D R, additional, Gronemeyer, H, additional, Hajnóczky, G, additional, Hardwick, J M, additional, Hengartner, M O, additional, Ichijo, H, additional, Jäättelä, M, additional, Kepp, O, additional, Kimchi, A, additional, Klionsky, D J, additional, Knight, R A, additional, Kornbluth, S, additional, Kumar, S, additional, Levine, B, additional, Lipton, S A, additional, Lugli, E, additional, Madeo, F, additional, Malorni, W, additional, Marine, J-CW, additional, Martin, S J, additional, Medema, J P, additional, Mehlen, P, additional, Melino, G, additional, Moll, U M, additional, Morselli, E, additional, Nagata, S, additional, Nicholson, D W, additional, Nicotera, P, additional, Nuñez, G, additional, Oren, M, additional, Penninger, J, additional, Pervaiz, S, additional, Peter, M E, additional, Piacentini, M, additional, Prehn, J H M, additional, Puthalakath, H, additional, Rabinovich, G A, additional, Rizzuto, R, additional, Rodrigues, C M P, additional, Rubinsztein, D C, additional, Rudel, T, additional, Scorrano, L, additional, Simon, H-U, additional, Steller, H, additional, Tschopp, J, additional, Tsujimoto, Y, additional, Vandenabeele, P, additional, Vitale, I, additional, Vousden, K H, additional, Youle, R J, additional, Yuan, J, additional, Zhivotovsky, B, additional, and Kroemer, G, additional

Published
2009
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46. Maturation Phenomenon in Cerebral Ischemia IV

Author

NAVAL MEDICAL RESEARCH CENTER SILVER SPRING MD, Bazan, N. G., Ito, U., Marcheselli, V. L., Kuroiwa, T., Klatzo, I., NAVAL MEDICAL RESEARCH CENTER SILVER SPRING MD, Bazan, N. G., Ito, U., Marcheselli, V. L., Kuroiwa, T., and Klatzo, I.

Abstract

Young animals were previously shown to be more resistant to ischemia than were adult animals. This difference was attributed to maturation/function of gonads and/or neurons. This study evaluated the existence of age-related changes in transcriptional expression of HSC70, HSP72, and c-fos mRNA intransient global ischemia, and their possible relationship to neuronal cell survival in CA1 hippocampus. The results indicated that ischemic response in young animals compared with that in adult animals showed: (1) more rapid and /or prolonged expression of HSC70, HSP72, and c-fos mRNAs; (2) a marked induction of HSP72 protein; and (3) enhanced pyramidal cell survival. The observed endogenous 'tolerance' of CA1 neurons in young gerbils to ischemia/reperfusion injury may be related to the expression of HSC70, HSP72 and c-fos.

Published
2001

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