ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Deletion of caveolin-1 protects hyperoxia-induced apoptosis via survivin-mediated pathways.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- 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
- ASK1 Regulates Bleomycin-induced Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Amelioration of Endotoxin-Induced Acute Lung Injury and Alveolar Epithelial Cells Apoptosis by Simvastatin Is Associated with Up-Regulation of Survivin/NF-kB/p65 Pathway.International journal of molecular sciences · 2022Article
- Protective effect of thymoquinone against lung intoxication induced by malathion inhalation.Scientific reports · 2021Article
- Striatin translocates to the cytosol of apoptotic cells and is proteolytically cleaved in a caspase 3-dependent manner.Heliyon · 2020Article
- miR‑21‑5p regulates type II alveolar epithelial cell apoptosis in hyperoxic acute lung injury.Molecular medicine reports · 2018Article
- Qi-Dong-Huo-Xue-Yin Inhibits Inflammation in Acute Lung Injury in Mice via Toll-Like Receptor 4/Caveolin-1 Signaling.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Inhibition of Caveolae Contributes to Propofol Preconditioning-Suppressed Microvesicles Release and Cell Injury by Hypoxia-Reoxygenation.Oxidative medicine and cellular longevity · 2017Article
- Increased caveolin-1 in intervertebral disc degeneration facilitates repair.Arthritis research & therapy · 2016Article
- TRIM72 modulates caveolar endocytosis in repair of lung cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Role of GDF15 (growth and differentiation factor 15) in pulmonary oxygen toxicity.Toxicology in vitro : an international journal published in association with BIBRA · 2015Article
- Article
- Caveolin-1 is a negative regulator of tumor growth in glioblastoma and modulates chemosensitivity to temozolomide.Cell cycle (Georgetown, Tex.) · 2013Article
- Flotillin-2 modulates fas signaling mediated apoptosis after hyperoxia in lung epithelial cells.PloS one · 2013Article
- Article
- NALP-3 inflammasome silencing attenuates ceramide-induced transepithelial permeability.Journal of cellular physiology · 2012Article
- Caveolin-1 inhibits expression of antioxidant enzymes through direct interaction with nuclear erythroid 2 p45-related factor-2 (Nrf2).The Journal of biological chemistry · 2012Article
- Absence of caveolin-1 alters heat shock protein expression in spontaneous mammary tumors driven by Her-2/neu expression.Histochemistry and cell biology · 2012Article
- Regulation and function of the two-pore-domain (K2P) potassium channel Trek-1 in alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Caveolin-1 mediates Fas-BID signaling in hyperoxia-induced apoptosis.Free radical biology & medicine · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Hyperoxia-induced lung injury is an established model that mimics human acute respiratory distress syndrome. Cell death is a prominent feature in lungs following prolonged hyperoxia. Caveolae are omega-shaped invaginations of the plasma membrane. Caveolin-1 (cav-1), a 22-kDa transmembrane scaffolding protein, is the principal structural component of caveolae. We have recently shown that deletion of cav-1 (cav-1-/-) protected against hyperoxia-induced cell death and lung injury both in vitro and in vivo; however, the mechanisms remain unclear. Survivin, a member of the inhibitor of apoptosis protein family, inhibits apoptosis in tumor cells. Although emerging evidence suggests that survivin is involved in wound healing, especially in vascular injuries, its role in hyperoxia-induced lung injury has not been investigated. Our current data demonstrated that hyperoxia induced apoptosis via suppressing survivin expression. Deletion of cav-1 abolished this suppression and subsequently protected against hyperoxia-induced apoptosis. Using "gain" and "loss" of function assays, we determined that survivin protected lung cells from hyperoxia-induced apoptosis via the inhibition of apoptosis executor caspase-3. Overexpression of survivin by deletion of cav-1 was regulated by Egr-1. Egr-1 functioned as a negative regulator of survivin expression. Deletion of cav-1 upregulated survivin via decreased Egr-1 binding of the survivin promoter region. Together, this study illustrates the effect of hyperoxia on survivin expression and the role of survivin in hyperoxia-induced apoptosis. We also demonstrate that deletion of cav-1 protects hyperoxia-induced apoptosis via modulation of survivin expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.