ArticleExperimental lung research2011
Bcl-X(L) is the primary mediator of p21 protection against hyperoxia-induced cell death.
Article in Experimental lung research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- p21Cancers · 2024Article
- Burn-Induced Apoptosis in the Livers of Aged Mice Is Associated With Caspase Cleavage of Bcl-xL.The Journal of surgical research · 2023Article
- Impaired Autophagic Activity Contributes to the Pathogenesis of Bronchopulmonary Dysplasia. Evidence from Murine and Baboon Models.American journal of respiratory cell and molecular biology · 2020Article
- Dysregulated autophagy in muscle precursor cells from humans with type 2 diabetes.Scientific reports · 2019Article
- The cardiomyocyte "redox rheostat": Redox signalling via the AMPK-mTOR axis and regulation of gene and protein expression balancing survival and death.Journal of molecular and cellular cardiology · 2019Article
- Article
- p21 induction plays a dual role in anti-cancer activity of ursolic acid.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin Triggered Resolvin D1 Treatment.American journal of respiratory cell and molecular biology · 2015Article
- MicroRNA-302 induces proliferation and inhibits oxidant-induced cell death in human adipose tissue-derived mesenchymal stem cells.Cell death & disease · 2014Article
- IκBβ-mediated NF-κB activation confers protection against hyperoxic lung injury.American journal of respiratory cell and molecular biology · 2014Article
- Carotid body growth during chronic postnatal hyperoxia.Respiratory physiology & neurobiology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A tight balance between anti- and proapoptotic members of the Bcl-2 family controls cell survival and death. Exposure to hyperoxia shifts this balance towards a prodeath state that ultimately activates Bak- and Bax-dependent cell death. Mechanisms underlying this shift are undefined; however, the cell cycle inhibitor p21 delays the loss of antiapoptotic Mcl-1 and Bcl-X(L), and protects against hyperoxia. Here, H1299 human lung adenocarcinoma cells are used to investigate how these and other members of the Bcl-2 family cooperate with p21 to protect against hyperoxia. Expression of antiapoptotic Mcl-1 and Bcl-X(L), but not Bcl-2 or A1, declined during hyperoxia, whereas proapoptotic Bak, but not Bax, increased. Conditional overexpression of p21 selectively delayed the loss of Mcl-1 and Bcl-X(L), without affecting expression of the other members. siRNA knockdown of Mcl-1 and Bcl-X(L) sensitized cells to hyperoxia, but only the loss of Bcl-X(L) ablated the protective effects of p21. Conversely, overexpression of Mcl-1 and Bcl-X(L) protected against hyperoxia, but only Bcl-X(L) bound Bak and Bax. Altogether, these data suggest that Bcl-X(L) is the primary mediator by which p21 protects against hyperoxia-induced Bak/Bax-dependent cell death.
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