The current study suggests that the upregulation of TGF-β1 may be associated with the downregulation of miR-663 in nasal polyposis in children. miR-663 may have regulatory effects on the pathogenesis of nasal polyposis by regulating TGF-β1 and may be developed as a genetic marker of nasal polyposis in children.
To investigate the potential role of vitamin D (1,25(OH)<sub>2</sub>D<sub>3</sub>) in preventing the development of nasal polyps, we examined the effect of vitamin D on myofibroblast differentiation and extracellular matrix (ECM) production in TGF-β1-induced nasal polyp-derived fibroblasts (NPDFs) and elucidated the mechanisms underlying its inhibitory effect.
Messenger RNA levels of TGF-β1, TGF-β receptor I, and Smad3 in CRSwNP ethmoid bone tissues were significantly higher than those in ethmoid bone tissues of patients with CRSsNP and the controls.
The levels of IL-6, IL-2, pSTAT3, pSTAT5, SOCS3, RORc, Foxp3, IL-17A, and TGF-β1 were measured in patients with atopic NP, patients with nonatopic NP, and controls.
Our conclusions were that that VEGFA and TGFbeta1 participate significantly in the formation of NPs, whereas FGF2 and IGF1 are implicated in nasal polyposis to a lesser, but still significant, extent.
We believe that the high expression of TGF-beta1 in inflammatory mucosa compared with the low expression in polyps may reflect an important role in the inhibitory mechanisms of nasal polyposis.
The aim of this study was to evaluate the role of MMPs and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in association with TGF-beta1, eosinophils and mast cell activation in nasal polyp tissue.