Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Jul 18;9(1):418.
doi: 10.1038/s41597-022-01470-8.

Transcriptomic study of anastasis for reversal of ethanol-induced apoptosis in mouse primary liver cells

Ho Man Tang  1   2 , C Conover Talbot Jr  3 , Ming Chiu Fung  4 , Ho Lam Tang  5
Affiliations

Transcriptomic study of anastasis for reversal of ethanol-induced apoptosis in mouse primary liver cells

Ho Man Tang et al. Sci Data. .

Abstract

Anastasis is a cell recovery mechanism that rescues dying cells from the brink of death. Reversal of apoptosis is the first example of anastasis. Here, we describe a comprehensive dataset containing time-course mRNA expression profiles for reversal of ethanol-induced apoptosis in mouse primary liver cells in νitro. This transcriptome dataset includes the conditions of the untreated cells, cells undergoing apoptosis triggered by incubating with cell death inducer of 4.5% ethanol for 5 hours, and apoptosis reversal of ethanol-induced cells at the early (3rd hour), middle (6th hour), and late (24th, 48th hour) stages after being washed with and incubated in fresh cell culture medium. By comparing this dataset with the transcriptomic profiles of other anastasis models generated with different combinations of cell types and cell death inducers, investigators can identify the key regulators governing reversal of apoptosis and other reversible cell death processes. Therefore, reusing or reanalysing this dataset will facilitate the future studies on the physiological, pathological, and therapeutic implications of anastasis.

PubMed Disclaimer

Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Overview of experimental design and study workflow. (a) Reversal of ethanol-induced apoptosis in mouse primary liver cells in νitro served as a model for this microarray study. Phase-contrast images of (i) untreated cells, (ii) cells undergoing apoptosis triggered by 4.5% ethanol (EtOH) for 5 hours, and (iii) ethanol-treated cells washed with and then incubated in fresh medium for 24 hours. (i’-iii’) Merged confocal images, with conditions like i-iii, for visualizing mitochondria (red), nuclei (blue), and cell morphology (DIC). (b) An outline of the workflow for the time-course microarray study. Mouse primary liver cells were treated with 4.5% ethanol for 5 hours to induce apoptosis (R0), and then were washed with and further incubated in fresh culture medium for 3 hours (R3), 6 hours (R6), 24 hours (R24), and 48 hours (R48) to allow reversal of apoptosis. Untreated cells served as control (Ctrl). Cell samples of three biological replicates from each condition mentioned above were collected for RNA extraction, analysed using Illumina Mouse WG-6 v2.0 Expression BeadChip for whole-genome expression profiling, and performed quality check by Partek Genomics Suite (GS) v6.6.
Fig. 2
Fig. 2
RNA integrity measurement. (a) A summary of RNA integrity numbers (RINs), (b) gel-like images, and (c–h) electropherograms generated by the Agilent 2100 Bioanalyzer system for determining the quality of the eighteen RNA samples (six conditions as listed in Fig. 1, three replicates for each condition). The six conditions are the untreated liver cells (ctrl), apoptotic liver cells induced with 4.5% ethanol for 5 hours (R0), and anastatic liver cells after removal of ethanol for 3 hours (R3), 6 hours (R6), 24 hours (R24), and 48 hours (R48). The 18 S and 28 S ribosomal bands are marked on the electropherograms. Fluorescence unit: FU; Time in second: S.
Fig. 3
Fig. 3
Quality check dataset. (a) Signal box plot illustrating the raw data distribution of eighteen samples in the dataset, depicting the log2 value of probe signal intensity of median, interquartile range, and whiskers of each sample. (b) Dendrogram of all eighteen samples’ raw log2 signals generated using hierarchical clustering. (c) Signal intensity of hepatic marker genes (Acly, Acta2, Dlk1), cardiac marker genes (Myh6, Myh7, Nppa), neural marker genes (Gad1, Sox1, and Sox2), and pancreatic marker genes (Nkx2-2, Nkx6-1, Pdx1) of eighteen samples in the dataset. Dotted line indicates the overall average signal in the dataset (log2 7.3).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Green DR, Amarante-Mendes GP. The point of no return: mitochondria, caspases, and the commitment to cell death. Results Probl Cell Differ. 1998;24:45–61. doi: 10.1007/978-3-540-69185-3_3. - DOI - PubMed
    1. Riedl SJ, Shi Y. Molecular mechanisms of caspase regulation during apoptosis. Nat Rev Mol Cell Biol. 2004;5:897–907. doi: 10.1038/nrm1496. - DOI - PubMed
    1. Chipuk JE, Bouchier-Hayes L, Green DR. Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario. Cell Death Differ. 2006;13:1396–402. doi: 10.1038/sj.cdd.4401963. - DOI - PubMed
    1. Holland AJ, Cleveland DW. Chromoanagenesis and cancer: mechanisms and consequences of localized, complex chromosomal rearrangements. Nat Med. 2012;18:1630–8. doi: 10.1038/nm.2988. - DOI - PMC - PubMed
    1. Bock FJ, Tait SWG. Mitochondria as multifaceted regulators of cell death. Nature Reviews Molecular Cell Biology. 2020;21:85–100. doi: 10.1038/s41580-019-0173-8. - DOI - PubMed

Publication types