OBJECTIVE: To investigate the role and mechanism of bombesin receptor subtype 3 (BRS-3) in the proliferation and protection against injury of human brochial epithelial cells (HBECs). METHODS: Effect of P3513 (a specific agonist of BRS-3) on the proliferation of HBECs was observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method; the release rate of 3H-Udr, and LDH activity, catalase activity, and the expression of cadherin and integrin beta1 were also analyzed under O3 stress with or without P3513 treatment. RESULTS: The proliferation of HBECs was accelerated by P3513 in a concentration-dependent manner (10(-9) approximately 10(-7) mol/L). Ozone stress could promote the release rate of 3H-Udr, and LDH activity, which could be inhibited by P3513. P3513 could promote the activity of catalase. The effect of proliferation and protection against injury caused by P3513 could be inhibited by W7 (calmodulin inhibitor), PD98059 (tyrosin kinase inhibitor) and H89 (PKA inhibitor). P3513 could stimulate the expression of caderin and integrinbeta1 of ozone-stressed HBECs. CONCLUSION: Activation of BRS-3 caused by P3513 may play an important role in protecting HBECs from oxidant injury, and the signal pathway is possibly relevant to Ca2+, MEK and PKA.
OBJECTIVE: To investigate the role and mechanism of bombesin receptor subtype 3 (BRS-3) in the proliferation and protection against injury of human brochial epithelial cells (HBECs). METHODS: Effect of P3513 (a specific agonist of BRS-3) on the proliferation of HBECs was observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method; the release rate of 3H-Udr, and LDH activity, catalase activity, and the expression of cadherin and integrin beta1 were also analyzed under O3 stress with or without P3513 treatment. RESULTS: The proliferation of HBECs was accelerated by P3513 in a concentration-dependent manner (10(-9) approximately 10(-7) mol/L). Ozone stress could promote the release rate of 3H-Udr, and LDH activity, which could be inhibited by P3513. P3513 could promote the activity of catalase. The effect of proliferation and protection against injury caused by P3513 could be inhibited by W7 (calmodulin inhibitor), PD98059 (tyrosin kinase inhibitor) and H89 (PKA inhibitor). P3513 could stimulate the expression of caderin and integrinbeta1 of ozone-stressed HBECs. CONCLUSION: Activation of BRS-3 caused by P3513 may play an important role in protecting HBECs from oxidant injury, and the signal pathway is possibly relevant to Ca2+, MEK and PKA.