ArticleFree radical biology & medicine2011
Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Cisplatin as a Xenobiotic Agent: Molecular Mechanisms of Actions and Clinical Applications in Oncology.Journal of xenobiotics · 2026Review
- Development of an acute lung injury model for drug testing.Scientific reports · 2025Article
- HMSCs exosome-derived miR-199a-5p attenuates sulfur mustard-associated oxidative stress via the CAV1/NRF2 signalling pathway.Journal of cellular and molecular medicine · 2023Article
- Dose-dependent effects of human umbilical cord-derived mesenchymal stem cell treatment in hyperoxia-induced lung injury of neonatal rats.Frontiers in pediatrics · 2023Article
- Caveolin-1 suppresses tumor formation through the inhibition of the unfolded protein response.Cell death & disease · 2020Article
- Upregulation of caveolin-1 and its colocalization with cytokine receptors contributes to beta cell apoptosis.Scientific reports · 2019Article
- Caveolin-1 Regulates P2YBiomolecules · 2019Article
- Overview of Crosstalk Between Multiple Factor of Transcytosis in Blood Brain Barrier.Frontiers in neuroscience · 2019Review
- Impairment of Fas-ligand-caveolin-1 interaction inhibits Fas-ligand translocation to rafts and Fas-ligand-induced cell death.Cell death & disease · 2018Article
- DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- MiR-15a/16 Regulates Apoptosis of Lung Epithelial Cells after Oxidative Stress.Molecular medicine (Cambridge, Mass.) · 2016Article
- Inflammatory cytokines induce caveolin-1/β-catenin signalling in rat nucleus pulposus cell apoptosis through the p38 MAPK pathway.Cell proliferation · 2016Article
- Lung epithelial cell-derived extracellular vesicles activate macrophage-mediated inflammatory responses via ROCK1 pathway.Cell death & disease · 2015Article
- Tagging strategies strongly affect the fate of overexpressed caveolin-1.Traffic (Copenhagen, Denmark) · 2015Article
- Bisdemethoxycurcumin Induces apoptosis in activated hepatic stellate cells via cannabinoid receptor 2.Molecules (Basel, Switzerland) · 2015Article
- A Frame-Shift Mutation in CAV1 Is Associated with a Severe Neonatal Progeroid and Lipodystrophy Syndrome.PloS one · 2015Article
- Luteolin induces apoptosis by activating Fas signaling pathway at the receptor level in laryngeal squamous cell line Hep-2 cells.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2014Article
- Interaction of caveolin-1 with ATG12-ATG5 system suppresses autophagy in lung epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Suppression of PTRF alleviates the polymicrobial sepsis induced by cecal ligation and puncture in mice.The Journal of infectious diseases · 2013Article
- Caveolin-1 is a negative regulator of tumor growth in glioblastoma and modulates chemosensitivity to temozolomide.Cell cycle (Georgetown, Tex.) · 2013Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Fas-mediated apoptosis is a crucial cellular event. Fas, the Fas-associated death domain, and caspase 8 form the death-inducing signaling complex (DISC). Activated caspase 8 mediates the extrinsic pathways and cleaves cytosolic BID. Truncated BID (tBID) translocates to the mitochondria, facilitates the release of cytochrome c, and activates the intrinsic pathways. However, the mechanism causing these DISC components to aggregate and form the complex remains unclear. We found that Cav-1 regulated Fas signaling and mediated the communication between extrinsic and intrinsic pathways. Shortly after hyperoxia (4 h), the colocalization and interaction of Cav-1 and Fas increased, followed by Fas multimer and DISC formation. Deletion of Cav-1 (Cav-1-/-) disrupted DISC formation. Further, Cav-1 interacted with BID. Mutation of Cav-1 Y14 tyrosine to phenylalanine (Y14F) disrupted the hyperoxia-induced interaction between BID and Cav-1 and subsequently yielded a decreased level of tBID and resistance to hyperoxia-induced apoptosis. The reactive oxygen species (ROS) scavenger N-acetylcysteine decreased the Cav-1-Fas interaction. Deletion of glutathione peroxidase-2 using siRNA aggravated the BID-Cav-1 interaction and tBID formation. Taken together, these results indicate that Cav-1 regulates hyperoxia/ROS-induced apoptosis through interactions with Fas and BID, probably via Fas palmitoylation and Cav-1 Y14 phosphorylation, respectively.
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Registered trials
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