[The role of Smad signaling pathway in the repair of mucosal epithelium in chronic sinusitis with nasal polyps and without nasal polyps].

Objective: To evaluate the differences in CRS and normal subjects between chronic rhinosinusitis without nasal polys (CRSsNP) and chronic rhinosinusitis with nasal polys (CRSwNP) in the role of TGF-β-Smad pathways in the repair of mucosal epithelium. Method: Ethmoidal mucosal samples collected from CRS and healthy control patients were analyzed for TGF-β1, TGF-β receptorⅠ,TGF-β receptor Ⅱ, Smad3, phospho-Smad3, Smad7, and Smad anchor for receptor activation by Western blot. The proliferation of sinonasal epithelial cells at baseline after TGF-β1 and/or EGF stimulation was evaluated by the MTT assay. Result: In CRSsNP,TGF-β1,TGF-β receptorⅠ,TGF-β receptor Ⅱ and Smad3 protein levels were significantly higher than controls. In CRSwNP, TGF-β1, Smad3 and pSmad3 protein levels were significantly lower than controls. Smad7 protein was significantly higher in CRS than controls. In vitro experiments demonstrated that the baseline proliferation levels of sinonasal epithelial cells were lower in CRS than controls. Conclusion: CRSwNP is characterized by a lower level of TGF-signaling compared with the control. In CRSsNP, although the upstream signaling of TGF-β was enhanced, over expression of Smad7 protein may restrain the downstream signaling components (e.g., pSmad3) and the TGF-β antiproliferative effect on sinonasal epithelium. The difference in the local tissue concentration of TGF-β1 between CRSsNP and CRSwNP patients did not show significant differences in epithelial proliferation.