Necrotic Cell Death in Response to Oxidant Stress Involves the Activation of the Apoptogenic Caspase-8/Bid Pathway
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Human epithelial (A549) cells exposed to hyperoxia die by cellular necrosis. In the current study, we demonstrated the involvement of apoptogenic factors in epithelial cell necrosis in response to hyperoxia, including the formation of the Fas-related death-inducing signaling complex and initiation of mitochondria-dependent apoptotic pathways. We showed increased activation of both Bid and Bax in A549 cells subjected to hyperoxia. Bax activation involved a Bid-assisted conformational change. We discovered that the response to hyperoxia in vivo predominantly involved the activation of the Bid/caspase-8 pathway without apparent increases in Bax expression. Disruption of the Bid pathway by gene deletion protected against cell death in vivo and in vitro. Likewise, inhibition of caspase-8 by Flip also protected against cell death. Taken together, we have demonstrated the involvement of apoptogenic factors in epithelial cell responses to hyperoxia, despite a final outcome of cellular necrosis. We have, for the first time, identified a predominant role for the caspase-8/Bid pathway in signaling associated with hyperoxic lung injury and cell death in vivo and in vitro.
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The antitumor effect of atmospheric hyperoxia may be due to oxidative stress and increased apoptosis (Bax/Bcl-2 mRNA expression rate), associated with the MAPK pathway.
“The antitumor effect of atmospheric hyperoxia may be due to oxidative stress and increased apoptosis (BCL2‐associated X [Bax]/Bcl‐2 mRNA expression rate), which is associated with the mitogen‐activated protein kinase (MAPK) pathway.”
From Hypoxia signaling in cancer: Implications for therapeutic interventions (2023) · cites this paper as [299]
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- Authors
- Wang, X., Ryter, S. W., Dai, C., Tang, Z.-L., Watkins, S. C., Yin, X.-M., Song, R., & Choi, A. M. K.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Choi, Augustine M.K.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-08
- Volume
- 278
- Issue
- 31
- Pages
- 29184-29191
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2052913152
- Cited by
- 136
- References
- 41
- Citations by year
- 2026: 3 · 2024: 3 · 2023: 4 · 2022: 2 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 4 · 2016: 2 · 2015: 2 · 2014: 4 · 2013: 5 · 2012: 2
- FWCI
- 5.08
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r01ai042365-02)
- National Heart, Lung, and Blood Institute (R01HL055330, R01HL55330, R01HL60234, R01HL060234)
- National Institute of Allergy and Infectious Diseases (R01 AI-42365)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- necrosis, hyperoxia, oxidative stress, caspase-8, Bid, Bax, mitochondrial apoptosis, A549 cells, epithelial cells, hyperoxic lung injury, c-FLIP
- MeSH terms
- Adenocarcinoma, Animals, Carrier Proteins, Cells, Cultured, Enzyme Inhibitors, Fibroblasts, Humans, Lung, Lung Neoplasms, Male, Membrane Glycoproteins, Mice, Inbred C3H, Mice, Inbred C57BL, Oxygen, Tumor Cells, Cultured, Apoptosis, Gene Deletion, Mice, Knockout, Oxidative Stress, fas Receptor, Caspases, Intracellular Signaling Peptides and Proteins, BH3 Interacting Domain Death Agonist Protein, Mice, Caspase 8, Fas Ligand Protein, CASP8 and FADD-Like Apoptosis Regulating Protein, Caspase 9, Caspase Inhibitors
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