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This Article Full Text Full Text (PDF) All Versions of this Article: 286/1/L165    most recent 00436.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Shan, L. Articles by Sunday, M. E. Search for Related Content PubMed PubMed Citation Articles by Shan, L. Articles by Sunday, M. E.

Bombesin-like peptide receptor gene expression, regulation, and function in fetal murine lung

¹Department of Pathology, Children's and Brigham and Women's Hospitals and Harvard Medical School, and ²Department of Medicine, Children's Hospital, Boston, Massachusetts 02115; ³Department of Pediatrics, Harbor-UCLA Research and Educational Institute, Torrance, California 90502; ⁴Department of Degenerative Neurological Diseases, National Institute of Neuroscience, Tokyo 187-8502; and ⁵Japan Society for the Promotion of Science, Tokyo 102-8471, Japan

Submitted 18 December 2002 ; accepted in final form 31 July 2003

Bombesin-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 (GRP)/bombesin-preferring receptor (GRPR), neuromedin B (NMB) receptor (NMBR), and the orphan bombesin receptor subtype-3 (BRS-3)], we analyzed the ontogeny of GRPR, NMBR, and BRS-3 gene expression in mouse lung. We examined the regulation of these three genes by dexamethasone and bombesin, which modulate lung development. Using incorporation of [³H]thymidine and [³H]choline, we then assessed whether GRP, NMB, and Leu⁸-phyllolitorin modulate lung growth and maturation in fetal lung explants. GRPR gene expression was detected predominantly in utero, whereas NMBR and BRS-3 genes were expressed from embryonic days 13–16 and on multiple postnatal days. All three mRNAs are present in airway epithelium and mesenchymal cells but occur in different relative patterns. These genes were regulated differently. Dexamethasone and bombesin increased GRPR mRNA, bombesin downregulated NMBR, and neither agent affected BRS-3. GRP increased incorporation of [³H]thymidine and [³H]choline in explants, whereas NMB induced cell proliferation and Leu⁸-phyllolitorin 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.

gastrin-releasing peptide; neuromedin B; bombesin receptor subtype 3; dexamethasone; cell proliferation; type II cell differentiation

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