Molecular signature of anastasis for reversal of apoptosis

We recently discovered an unexpected reversibility of execution-stage apoptosis in vitro and in vivo, and coined the term anastasis (Greek for “rising to life”) for this cell recovery phenomenon. Promoting anastasis could in principle preserve injured cells that are difficult to replace such as cardiomyocytes and neurons. Conversely, arresting anastasis in dying cancer cells after cancer therapies could improve treatment efficacy. To harness the discovery of anastasis to develop revolutionary new therapies, it is essential to identify the key regulators of anastasis – the therapeutic targets. Therefore, we performed microarray analysis to study the molecular mechanism of anastasis using reversal of ethanol-induced apoptosis in mouse primary liver cells as a model. Our data reveal active transcription involved in multiple pathways during anastasis, including early activation of pro-survival genes, cell cycle arrest, anti-p53-mediated DNA damage response, and at delayed times, stress-inducible responses such as cell migration. Here, we present a dataset containing the time-course gene expression profiles during apoptosis reversal, which has implications for the physiological, pathological, and therapeutic implications of anastasis. Mouse primary liver cells were treated with 4.5% ethanol for 5 hours (0 hour timepoint) and then washed and cultured in fresh medium for 3, 6, 24, and 48 hours. Three biological replicates were analyzed for each of 6 timepoints: pre-ethanol treament (Ctrl), 0 hours (R0), 3 hours (R3), 6 hours (R6), 24 hours (R24), and 48 hours (R48).