Wound repair and proliferation of bronchial epithelial cells enhanced by bombesin receptor subtype 3 activation.

Abstract

The present study was designed to investigate the role of bombesin receptor subtype 3 (BRS-3) in airway wound repair. The results showed that: (1) There was few expression of BRS-3 mRNA in the control group. In contrast, the expression of BRS-3 mRNA was gradually increased in the early 2 days, and peaked on the fourth day, and then decreased in the ozone-stressed AHR animal. BRS-3 mRNA was distributed in the ciliated columnar epithelium, monolayer columnar epithelium cells, scattered mesenchymal cells and Type II alveolar cells; (2) The wound repair and proliferation of bronchial epithelial cells (BECs) were accelerated in a concentration-dependent manner by BRS-3 activation with P3513, which could be inhibited by PKA inhibitor H89. The study demostrated that activation of BRS-3 may play an important role in wound repair of AHR.

• Authors: Yu-Rong Tan, Ming-Ming Qi, Xiao-Qun Qin, Yang Xiang, Xiang Li, Yue Wang, Fei Qu, Hui-Jun Liu, Jian-Song Zhang
• Journal: Peptides (Peptides) Vol. 27 Issue 7 Pg. 1852-8 (Jul 2006) ISSN: 0196-9781 [Print] United States
• PMID: 16426703 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Enzyme Inhibitors
• Isoquinolines
• Receptors, Bombesin
• Sulfonamides
• bombesin receptor subtype 3
• Cyclic AMP-Dependent Protein Kinase Type II
• Cyclic AMP-Dependent Protein Kinases
• N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide

Topics

• Animals
• Bronchi (metabolism)
• Cell Proliferation
• Cells, Cultured
• Cyclic AMP-Dependent Protein Kinase Type II
• Cyclic AMP-Dependent Protein Kinases (antagonists & inhibitors)
• Dose-Response Relationship, Drug
• Enzyme Inhibitors (pharmacology)
• Epithelial Cells (cytology)
• Isoquinolines (pharmacology)
• Mesoderm (metabolism)
• Microscopy, Video
• Rabbits
• Receptors, Bombesin (chemistry, metabolism)
• Sulfonamides (pharmacology)
• Wound Healing