The DOI matches its Crossref record; 52 of the 54 references it cites were found in a registry or an index.
Apoptosis or senescence-like growth arrest: influence of cell-cycle position, p53, p21 and bax in H2O2 response of normal human fibroblasts
Open accessAbstract
Early-passage human diploid fibroblasts (HDFs) undergo senescence-like growth arrest in response to sublethal concentrations of H2O2 [Chen and Ames (1994) Proc. Natl. Acad. Sci. U.S.A. 95, 4130-4134]. We determine here whether H2O2 can cause apoptosis in HDFs and the molecular changes that differ between apoptosis and senescence-like growth arrest. When exponentially growing early-passage IMR-90 cells were treated for 2 h with 50-200 μM (or 0.25-1 pmol/cell) H2O2, a fraction of cells detached at 16-32 h after the treatment. The cells remaining attached were growth-arrested and developed features of senescence in 1 week. The detached cells showed caspase-3 activation and typical morphological changes associated with apoptosis. Caspase-3 activation was H2O2 dose-dependent and preceded nuclear condensation or plasma membrane leakage. Apoptotic cells were mainly distributed in the S-phase of the cell cycle, while growth-arrested cells exhibited predominantly G1- and G2/M-phase distributions. H2O2 pretreatment induced G1 arrest and prohibited induction of apoptosis by a subsequent H2O2 challenge. The p53 protein showed an average 6.1-fold elevation in apoptotic cells and a 3.5-fold elevation in growth-arrested cells. Reduction of p53 levels with human papillomavirus E6 protein prohibited the activation of caspase-3 and decreased the proportion of apoptotic cells. Growth-arrested cells had elevated p21, while p21 was absent in apoptotic cells. Bcl-2 was elevated in both growth-arrested and apoptotic cells. Finally, although the overall level of bax did not change in growth-arrested or apoptotic cells, the solubility of bax protein increased in apoptotic cells. Our data suggest that in contrast with growth-arrested cells, apoptotic cells show an S-phase cell cycle distribution, a higher degree of p53 elevation, an absence of p21 protein and increased solubility of bax protein.
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“Indeed, induction of senescence appears protective against p53-dependent apoptosis [146] and high oxidative stress [254,255].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [254]
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Cellular response to oxidative stress: Signaling for suicide and survival*
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Negative Control of p53 by Sir2α Promotes Cell Survival under Stress
Luo, J., Nikolaev, A. Y., Imai, S.-I., Chen, D., Su, F., Shiloh, A., Guarente, L., & Gu, W. (2001) · Cell · doi:10.1016/s0092-8674(01)00524-4 · Cited by 2,081
Senescence and apoptosis: dueling or complementary cell fates?
Childs, B. G., Baker, D. J., Kirkland, J. L., Campisi, J., & van Deursen, J. M. (2014) · The EMBO Reports · doi:10.15252/embr.201439245 · Cited by 915
Boonstra, J., & Post, J. A. (2004) · Gene · doi:10.1016/j.gene.2004.04.032 · Cited by 737
Metadata
- Authors
- CHEN, Q. M., LIU, J., & MERRETT, J. B.
- Affiliations
- University of Arizona (US)
- ORCID
- CHEN, Qin M.
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2000-04-10
- Volume
- 347
- Issue
- 2
- Pages
- 543-551
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC1220988
- OpenAlex
- W1979962552
- Cited by
- 280
- References
- 54
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 6 · 2023: 8 · 2022: 8 · 2021: 18 · 2020: 9 · 2019: 9 · 2018: 8 · 2017: 10 · 2016: 7 · 2015: 9 · 2014: 11 · 2013: 9 · 2012: 6
- FWCI
- 9.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biochemical Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- apoptosis, hydrogen peroxide, human diploid fibroblasts, caspase-3 activation, p53, p21, Bax, Bcl-2, S phase, oxidative stress response
- MeSH terms
- Cell Cycle, Cell Membrane, Cell Nucleus, DNA, Dose-Response Relationship, Drug, Enzyme Activation, Fibroblasts, Flow Cytometry, Humans, Hydrogen Peroxide, Proto-Oncogene Proteins, Trypan Blue, Blotting, Western, Tumor Suppressor Protein p53, G1 Phase, Cyclins, Cellular Senescence, Apoptosis, Oxidative Stress, Proto-Oncogene Proteins c-bcl-2, Caspases, Cyclin-Dependent Kinase Inhibitor p21, bcl-2-Associated X Protein, Caspase 3
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- CoChat. (2026). Citation check: Apoptosis or senescence-like growth arrest: influence of cell-cycle position, p53, p21 and bax in H2O2 response of normal human fibroblasts. https://app.cochat.ai/papers/10.1042/bj3470543
- The paper
- CHEN, Q. M., LIU, J., & MERRETT, J. B. (2000). Apoptosis or senescence-like growth arrest: influence of cell-cycle position, p53, p21 and bax in H2O2 response of normal human fibroblasts. Biochemical Journal. https://doi.org/10.1042/bj3470543
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
