| pubmed-article:19880821 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C0221908 | lld:lifeskim |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C1160389 | lld:lifeskim |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C0030054 | lld:lifeskim |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C0547070 | lld:lifeskim |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C1332397 | lld:lifeskim |
| pubmed-article:19880821 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
| pubmed-article:19880821 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19880821 | pubmed:dateCreated | 2010-8-20 | lld:pubmed |
| pubmed-article:19880821 | pubmed:abstractText | Recent studies indicate that the antiapoptotic Bcl-X(L), one of five isoforms expressed by the Bcl-X gene, protects a variety of cell lines exposed to hyperoxia. However, its role in lung development and protection against oxidative stress in vivo is not known. Here, we show Bcl-X(L) is the predominant isoform expressed in the lung, and the only isoform detected in respiratory epithelium. Because loss of Bcl-X(L) is embryonically lethal, Bcl-X(L) was ablated throughout the respiratory epithelium by mating mice with a floxed exon II of the Bcl-X gene with mice expressing Cre under control of the surfactant protein-C promoter. Interestingly, the loss of Bcl-X(L) in respiratory epithelium was perinatally lethal in approximately 50% of the expected offspring. However, some adult mice lacking the gene were obtained. The epithelial-specific ablation of Bcl-X(L) did not disrupt pulmonary function, the expression of epithelial cell-specific markers, or lung development. However, it shifted the lung toward a proapoptotic state, defined by a reduction in antiapoptotic Mcl-1, an increase in proapoptotic Bak, and increased sensitivity of the respiratory epithelium to hyperoxia. Intriguingly, increased 8-oxoguanine lesions seen during hyperoxia were also evident as lungs transitioned to room air at birth, a time when perinatal lethality in some mice lacking Bcl-X(L) was observed. These findings reveal that the epithelial-specific expression of Bcl-X(L) is not required for proper lung development, but functions to protect respiratory epithelial cells against oxygen-induced toxicity, such as during hyperoxia and the lung's first exposure to ambient air. | lld:pubmed |
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| pubmed-article:19880821 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19880821 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19880821 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19880821 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19880821 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:19880821 | pubmed:issn | 1535-4989 | lld:pubmed |
| pubmed-article:19880821 | pubmed:author | pubmed-author:DeanDavid ADA | lld:pubmed |
| pubmed-article:19880821 | pubmed:author | pubmed-author:CallahanLinda... | lld:pubmed |
| pubmed-article:19880821 | pubmed:author | pubmed-author:O'ReillyMicha... | lld:pubmed |
| pubmed-article:19880821 | pubmed:author | pubmed-author:StaverskyRhon... | lld:pubmed |
| pubmed-article:19880821 | pubmed:author | pubmed-author:VitielloPeter... | lld:pubmed |
| pubmed-article:19880821 | pubmed:author | pubmed-author:YeeMinM | lld:pubmed |
| pubmed-article:19880821 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19880821 | pubmed:volume | 43 | lld:pubmed |
| pubmed-article:19880821 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19880821 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19880821 | pubmed:pagination | 376-85 | lld:pubmed |
| pubmed-article:19880821 | pubmed:dateRevised | 2011-9-13 | lld:pubmed |
| pubmed-article:19880821 | pubmed:meshHeading | pubmed-meshheading:19880821... | lld:pubmed |
| pubmed-article:19880821 | pubmed:meshHeading | pubmed-meshheading:19880821... | lld:pubmed |
| pubmed-article:19880821 | pubmed:meshHeading | pubmed-meshheading:19880821... | lld:pubmed |
| pubmed-article:19880821 | pubmed:meshHeading | pubmed-meshheading:19880821... | lld:pubmed |
