Strategies for tracking anastasis, a cell survival phenomenon that reverses apoptosis.
Anastasis (Greek for "rising to life") refers to the recovery of dying cells. Before these cells recover, they have passed through important checkpoints of apoptosis, including mitochondrial fragmentation, release of mitochondrial cytochrome c into the cytosol, activation of caspases, chromatin condensation, DNA damage, nuclear fragmentation, plasma membrane blebbing, cell shrinkage, cell surface exposure of phosphatidylserine, and formation of apoptotic bodies. Anastasis can occur when apoptotic stimuli are removed prior to death, thereby allowing dying cells to reverse apoptosis and potentially other death mechanisms. Therefore, anastasis appears to involve physiological healing processes that could also sustain damaged cells inappropriately. The functions and mechanisms of anastasis are still unclear, hampered in part by the limited tools for detecting past events after the recovery of apparently healthy cells. Strategies to detect anastasis will enable studies of the physiological mechanisms, the hazards of undead cells in disease pathology, and potential therapeutics to modulate anastasis. Here, we describe effective strategies using live cell microscopy and a mammalian caspase biosensor for identifying and tracking anastasis in mammalian cells.
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health; School of Life Sciences, Chinese University of Hong Kong; Center for Cell Dynamics, Department of Biological Chemistry, Johns Hopkins University School of Medicine; holamtang@jhmi.edu.
Ho Lam
HL
Tang
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health; School of Life Sciences, Chinese University of Hong Kong; Center for Cell Dynamics, Department of Biological Chemistry, Johns Hopkins University School of Medicine; homantang@jhmi.edu.
Ho Man
HM
Tang
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health.
J Marie
JM
Hardwick
School of Life Sciences, Chinese University of Hong Kong; mingchiufung@cuhk.edu.hk.
Ming Chiu
MC
Fung
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D019556:COS Cells; D020169:Caspases / Q000378:metabolism; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000502:physiology*; D058948:Cell Tracking / Q000379:methods*; D002522:Chlorocebus aethiops; D045304:Cytochromes c / Q000378:metabolism; D004249:DNA Damage; D005260:Female; D057809:HEK293 Cells; D006801:Humans; D008297:Male; D051379:Mice; D008928:Mitochondria / Q000378:metabolism; D041681:NIH 3T3 Cells; D010718:Phosphatidylserines / Q000494:pharmacology
D010718:Phosphatidylserines; D045304:Cytochromes c; D020169:Caspases