Abstract: Objective To explore effects of focal adhesion kinase on mucin(MUC)5AC hypersecretion induced by mechanical stress. Methods Normal human bronchial epithelial (NHBE) cells were cultured at an air-liquid interface and were exposed to chronic intermittent compressive mechanical stress via Transwell mechanical stress apparatus. Cells were treated with FAK siRNA. Western blot was performed to determine FAK and phosphorylation of ERK1/2 protein contents. Real-time PCR and ELISA were underwent to test MUC5AC mRNA and protein contents respectively. Results Relative expression level of phosphorylation of FAK at Tyr397 (p-FAK-Y397) in mechanical group was significantly higher than those in control group. Compared with the control group, mechanical stress could increase expressions of MUC5AC mRNA and protein contents significantly and also the protein expression of p-ERK1/2（P <0.01）. FAK siRNA could significantly attenuated the stress-induced increase in MUC5AC mRNA and protein expression and also the protein expression of p-ERK1/2（P <0.01）. But expressions of MUC5AC mRNA and protein and p-ERK1/2 protein in mechanical + FAK siRNA group were still higher than those in FAK siRNA control group（P <0.05）. PD98059 could significantly decrease the stress-induced increase in MUC5AC mRNA and protein expression（P <0.01）. Combination of FAK siRNA and AG1478 could significantly inhibit the stress-induced increase in MUC5AC mRNA and protein expression（P <0.01）. AG1478 alone could effectively decrease stress-induced increase in MUC5AC mRNA and protein expression（P <0.05），but when compared with AG1478 control group，differences were still significant. Conclusion The signal transduction pathway of stress-induced overexpression of MUC5AC is ERK-dependent，FAK is one of the upstream signal molecules of ERK.

Key words: focal adhesion kinase, mechanical stress, mucins, extracellular signal-regulated kinase