Wound repair and proliferation of bronchial epithelial cells enhanced by bombesin receptor subtype 3 activation.
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Tan YR, Qi MM, Qin XQ, Xiang Y, Li X, Wang Y, Qu F, Liu HJ, Zhang JS
Wound repair and proliferation of bronchial epithelial cells enhanced by bombesin receptor subtype 3 activation.
Peptides. 2006 Jul;27(7):1852-8. Epub 2006 Jan 19.
- PubMed ID
- 16426703 [ View in PubMed]
- 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.