Abstract
We previously demonstrated that bombesin-like peptide (BLP) mediates lung injury in premature infants with bronchopulmonary dysplasia (BPD). We now investigate gene expression and function of BLP (gastrin-releasing peptide, GRP) and BLP-receptors (GRP-R and BRS-3) in lung from two baboon BPD models. In the "interrupted gestation model," only GRP mRNA was up-regulated. In the "hyperoxic model," GRP-R mRNA was up-regulated. In lung explants from O2-treated animals, all BPD animals responded to 1nM bombesin, whereas non-BPD animals did not; the opposite effect was observed with a BLP blocking antibody. Cumulatively, these observations suggest that novel BLPs and/or BLP receptors are likely to be implicated in the pathogenesis of BPD.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Bombesin / metabolism
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Bombesin / pharmacology
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Dexamethasone / pharmacology
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Gastrin-Releasing Peptide / biosynthesis*
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Gastrin-Releasing Peptide / physiology*
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Gene Expression
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In Situ Hybridization
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Lung / embryology
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Lung / metabolism*
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Organ Culture Techniques
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Oxygen / metabolism
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Papio / metabolism*
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Phosphatidylcholines / pharmacology
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RNA, Messenger / metabolism
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Receptors, Bombesin / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Time Factors
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Up-Regulation*
Substances
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Phosphatidylcholines
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RNA, Messenger
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Receptors, Bombesin
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bombesin receptor subtype 3
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di-(8-methylstearoyl)phosphatidylcholine
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Dexamethasone
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Gastrin-Releasing Peptide
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Bombesin
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Oxygen