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[Relationship between the expression of tenascin C and TGF-beta1 in human nasal polyp tissues]
Zheng Liu1, Xue-jun you, Song Zhang
1Department of Otorhinolaryngology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Zhengliuent@hotmail.com
Objective:
To explore the mechanism underlying the increased expression of tenascin C (TNC) in human nasal polyp tissues.
Methods:
The method of immunohistochemistry was used to detect the protein expression of TNC and transforming growth factor-beta1 (TGF-beta1) and their relationship in nasal polyp tissues. The cell culture, real-time RT-PCR and in situ ELISA techniques were employed to investigate the effect of TGF-beta1 and eosinophils on the TNC mRNA and protein expression in BEAS-2B immortalized human bronchial epithelial cells.
Results:
(1) TNC and TGF-beta1 protein expression were up-regulated in nasal polyp tissues. TNC expression level was associated with the number of TGF-beta1 positive cells (r = -0.58, P < 0.01) and TGF-beta1 positive eosinophils (r = -0.61, P < 0.01); (2) 1 ng/ml and 10 ng/ml TGF-beta1 induced TNC mRNA expression by 7.20 +/- 3.43-fold and 22.48 +/- 5.35-fold (P < 0.01) in BEAS-2B cells after 4 h stimulation respectively. The fluorescence intensity of TNC protein expression was 129. 50 +/- 47.42 and 151.20 +/- 48.36 after 24 h stimulation respectively. The protein expression was significantly increased compared with that without stimulation (60.60 +/- 38.53, P < 0.05); (3) Coculture BEAS-2B cells and eosinophils at 2:1, 1:1 and 1:2 ratio, TNC mRNA expression was induced by 4.90 +/- 1.40-fold, 5.48 +/- 1.60-fold and 4.78 +/- 1.32-fold (P < 0.01) in BEAS-2B cells after 4 h coculture respectively. The fluorescence intensity of TNC protein expression was 128.75 +/- 44.15, 142.33 +/- 29.06 and 131.33 +/- 20.87 after 24 h coculture respectively. The protein expression was significantly increased compared with that without eosinophils coculture (59.40 +/- 10.14, P < 0.05). Treatment with neutralizing antibody to TGF-beta1 significantly inhibited eosinophil-induced BEAS-2B cells TNC expression in a dose-dependent manner (P < 0.05).
Conclusion:
TGF-beta1 and eosinophils can induce TNC expression in airway epithelial cells. The effect of eosinophils is partially mediated through TGF-beta1. Up-regulated expression of TNC in nasal polyp tissues is related to eosinophil-derived TGF-beta1.
