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1 Department of Pathology, Children's Hospital & Women's Hospital and Harvard Medical School, Boston, MA, USA
2 Department of Pathology, Children's Hospital & Women's Hospital and Harvard Medical School, Boston, MA, USA; Department of Medicine, Chirdren's Hospital, Boston, MA, USA
3 Department of Pediatrics, Harbor-UCLA Research and Educational Institute, Torrance, CA, USA
4 Department of Degenerative, National Institute of Neuroscience, Tokyo, Japan
5 Department of Degenerative, National Institute of Neuroscience, Tokyo, Japan; Japan Society for the Promotion of Science, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: sunday{at}tch.harvard.edu.
Bombesin-like peptide (BLP) immunoreactivity occurs at high levels in fetal lung. Previous studies showed that bombesin promotes fetal lung development. To test the hypothesis that such effects are mediated by known mammalian bombesin receptors [gastrin-releasing peptide/bombesin-preferring receptor (GRP-R), neuromedin B receptor (NMB-R), and the orphan bombesin receptor subtype-3 (BRS-3)], we analyzed the ontogeny of GRP-R, NMB-R, and BRS-3 gene expression in mouse lung. We examined regulation of these 3 genes by dexamethasone and bombesin, which modulate lung development. We then assessed whether GRP, NMB, and leu8-phyllolitorin modulate lung growth and maturation in fetal lung explants using 3H-thymidine and 3H-choline incorporation. GRP-R gene expression was detected predominantly in utero, whereas NMB-R and BRS-3 genes were expressed from E13-E16 and multiple postnatal days. All 3 mRNAs are present in airway epithelium and mesenchymal cells, but occur in different relative patterns. These genes were regulated differently. Both Dex and bombesin increased GRP-R mRNA, bombesin down-regulated NMB-R, and neither agent affected BRS-3. GRP increased 3H-thymidine and 3H-choline incorporation in explants, whereas NMB induced cell proliferation, and L8PL yielded variable results. Cumulative data suggest the involvement of multiple BLP receptors including novel molecules and argue against simple functional redundancy within this gene family during lung development.
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