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Bombesin and [Leu8]phyllolitorin promote fetal mouse lung branching morphogenesis via a receptor-mediated mechanism.

Publication ,  Journal Article
King, KA; Torday, JS; Sunday, ME
Published in: Proc Natl Acad Sci U S A
May 9, 1995

Pulmonary neuroendocrine cells are localized predominantly at airway branchpoints. Previous work showed that gastrin-releasing peptide (GRP), a major pulmonary bombesin-like peptide, occurred in neuroendocrine cells exclusively in branching human fetal airways. We now demonstrate that GRP and GRP receptor genes are expressed in fetal mouse lung as early as embryonic day 12 (E12), when lung buds are beginning to branch. By in situ hybridization, GRP receptor transcripts were at highest levels in mesenchymal cells at cleft regions of branching airways and blood vessels. To explore the possibility that bombesin-like peptides might play a role in branching morphogenesis, E12 lung buds were cultured for 48 hr in serum-free medium. In the presence of 0.10-10 microM bombesin, branching was significantly augmented as compared with control cultures, with a peak of 94% above control values at 1 microM (P < 0.005). The bombesin receptor antagonist [Leu13- psi(CH2NH)Leu14]bombesin alone (100 nM) had no effect on baseline branching but completely abolished bombesin-induced branching. A bombesin-related peptide, [Leu8]phyllolitorin also increased branching (65% above control values at 10 nM, P < 0.005). [Leu8]Phyllolitorin also significantly augmented thymidine incorporation in cultured lung buds. Fibronectin, which is abundant at branchpoints, induces GRP gene expression in undifferentiated cell lines. These observations suggest that BLPs secreted by pulmonary neuroendocrine cells may contribute to lung branching morphogenesis. Furthermore, components of branchpoints may induce pulmonary neuroendocrine cell differentiation as part of a positive feedback loop, which could account in part for the high prevalence of these cells at branchpoints.

Duke Scholars

Published In

Proc Natl Acad Sci U S A

DOI

ISSN

0027-8424

Publication Date

May 9, 1995

Volume

92

Issue

10

Start / End Page

4357 / 4361

Location

United States

Related Subject Headings

  • Transcription, Genetic
  • Receptors, Bombesin
  • Pyrrolidonecarboxylic Acid
  • Pregnancy
  • Polymerase Chain Reaction
  • Oligopeptides
  • Morphogenesis
  • Molecular Sequence Data
  • Mice, Inbred Strains
  • Mice
 

Citation

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King, K. A., Torday, J. S., & Sunday, M. E. (1995). Bombesin and [Leu8]phyllolitorin promote fetal mouse lung branching morphogenesis via a receptor-mediated mechanism. Proc Natl Acad Sci U S A, 92(10), 4357–4361. https://doi.org/10.1073/pnas.92.10.4357
King, K. A., J. S. Torday, and M. E. Sunday. “Bombesin and [Leu8]phyllolitorin promote fetal mouse lung branching morphogenesis via a receptor-mediated mechanism.Proc Natl Acad Sci U S A 92, no. 10 (May 9, 1995): 4357–61. https://doi.org/10.1073/pnas.92.10.4357.
King KA, Torday JS, Sunday ME. Bombesin and [Leu8]phyllolitorin promote fetal mouse lung branching morphogenesis via a receptor-mediated mechanism. Proc Natl Acad Sci U S A. 1995 May 9;92(10):4357–61.
King, K. A., et al. “Bombesin and [Leu8]phyllolitorin promote fetal mouse lung branching morphogenesis via a receptor-mediated mechanism.Proc Natl Acad Sci U S A, vol. 92, no. 10, May 1995, pp. 4357–61. Pubmed, doi:10.1073/pnas.92.10.4357.
King KA, Torday JS, Sunday ME. Bombesin and [Leu8]phyllolitorin promote fetal mouse lung branching morphogenesis via a receptor-mediated mechanism. Proc Natl Acad Sci U S A. 1995 May 9;92(10):4357–4361.
Journal cover image

Published In

Proc Natl Acad Sci U S A

DOI

ISSN

0027-8424

Publication Date

May 9, 1995

Volume

92

Issue

10

Start / End Page

4357 / 4361

Location

United States

Related Subject Headings

  • Transcription, Genetic
  • Receptors, Bombesin
  • Pyrrolidonecarboxylic Acid
  • Pregnancy
  • Polymerase Chain Reaction
  • Oligopeptides
  • Morphogenesis
  • Molecular Sequence Data
  • Mice, Inbred Strains
  • Mice