Source:http://linkedlifedata.com/resource/pubmed/id/21398497
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2011-6-3
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| pubmed:abstractText |
Adequate expression of surfactant protein-B (SP-B) is critical in the function of pulmonary surfactant to reduce alveolar surface tension. Expression of SP-B mRNA is restricted to specific lung-airway epithelial cells, and human SP-B mRNA stability is increased in the presence of the synthetic glucocorticoid dexamethasone (DEX). Although the mechanism of SP-B mRNA stabilization by DEX is unknown, studies suggest involvement of the glucocorticoid receptor (GR). We developed a dual-cistronic plasmid-based expression assay in which steady-state levels of SP-B mRNA, determined by Northern analysis, reproducibly reflect changes in SP-B mRNA stability. Using this assay, we found that steady-state levels of SP-B mRNA increased greater than twofold in transfected human-airway epithelial cells (A549) incubated with DEX (10(-7) M). DEX-mediated changes in SP-B mRNA levels required the presence of the SP-B mRNA 3'-untranslated region but did not require ongoing protein synthesis. The effect of DEX on SP-B mRNA levels was dose dependent, with maximal effect at 10(-7) M. DEX increased levels of SP-B mRNA in cells lacking GR, and the presence of the GR antagonist RU486 did not interfere with the effect of DEX. Surprisingly, other steroid hormones (progesterone, estradiol, and vitamin D; 10(-7) M) significantly increased SP-B mRNA levels, suggesting a common pathway of steroid hormone action on SP-B mRNA stability. These results indicate that the effect of DEX to increase SP-B mRNA stability is independent of activated GR and suggests that the mechanism is mediated by posttranscriptional or nongenomic effects of glucocorticoids.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Hormone Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Mifepristone,
http://linkedlifedata.com/resource/pubmed/chemical/Pulmonary Surfactant-Associated...,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jun
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| pubmed:issn |
1522-1504
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
300
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
L940-50
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| pubmed:meshHeading |
pubmed-meshheading:21398497-Anti-Inflammatory Agents,
pubmed-meshheading:21398497-Blotting, Northern,
pubmed-meshheading:21398497-Cells, Cultured,
pubmed-meshheading:21398497-Dexamethasone,
pubmed-meshheading:21398497-Endothelium, Vascular,
pubmed-meshheading:21398497-HeLa Cells,
pubmed-meshheading:21398497-Hormone Antagonists,
pubmed-meshheading:21398497-Humans,
pubmed-meshheading:21398497-Kidney,
pubmed-meshheading:21398497-Lung,
pubmed-meshheading:21398497-Mifepristone,
pubmed-meshheading:21398497-Pulmonary Surfactant-Associated Protein B,
pubmed-meshheading:21398497-RNA, Messenger,
pubmed-meshheading:21398497-RNA Processing, Post-Transcriptional,
pubmed-meshheading:21398497-RNA Stability,
pubmed-meshheading:21398497-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21398497-Transcription, Genetic,
pubmed-meshheading:21398497-Umbilical Veins
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| pubmed:year |
2011
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| pubmed:articleTitle |
Glucocorticoid regulation of human pulmonary surfactant protein-B (SP-B) mRNA stability is independent of activated glucocorticoid receptor.
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| pubmed:affiliation |
Department of Pediatrics, Division of Neonatal-Perinatal Medicine, University of Texas Health Sciences Center at Houston, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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