Chronic rhinosinusitis with nasal polyps (CRSwNP) is a persistent sinonasal mucosa inflammatory disease with still unclear pathophysiologic mechanisms that imply events of tissue repair and structural remodelling. Several cascades seem to have a considerable role in the onset and progression of mucosa hyperproliferation in nasal polyps including transforming growth factor β/Small mother against decapentaplegic (TGFβ/Smads), mitogenactivated protein kinases (MAPKs), advanced glycosylation end-products (AGEs) together with epithelial-tomesenchymal transition (EMT). Since many inflammatory mediators are reported to play important roles in the development of nasal polyps (NP) disease, this study aimed to analyse the correlation between the AGEs/receptor of advanced glycosylation end-products (RAGE)/extracellular signal-regulated kinase (ERK) signalling pathway and the main markers of EMT to better understand the influence that they exert on the remodelling of nasal mucous membranes in patients affected by CRSwNP vs normal controls. A total of 30 patients were enrolled in this study. Immunohistochemical analysis, using AGE, RAGE, p-ERK, MMP-3, TGF-β1, Smad2/3, Collagen I-III, α-SMA, E-cadherin, IL-6 and Vimentin antibodies, was performed. AGE, RAGE, ERK, p-ERK and MMP3 were also evaluated using western blot analysis. We observed an overexpression of the AGE/RAGE/p-ERK and the main mesenchymal markers of EMT (Vimentin and IL-6) in CRSwNP vs controls whereas the TGF-β/Smad3 pathway did not show any significant differences between the two groups of patients. These observations suggest a complex network of processes in the pathogenesis of NP, and the AGE/RAGE/ERK pathway and EMT might work together in promoting tissue remodelling in the formation of CRSwNP.

中文翻译：

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AGE / RAGE / ERK信号通路和上皮-间质转化是否可以在鼻息肉的慢性鼻-鼻窦炎的发病机理中相互作用？

慢性鼻-鼻息肉鼻窦炎（CRSwNP）是一种持续性鼻窦粘膜炎性疾病，其病理生理机制尚不明确，暗示组织修复和结构重塑。几个级联似乎在鼻息肉的粘膜过度增生的发生和发展中起着相当重要的作用，包括转化生长因子β/小母亲抵抗十足瘫痪（TGFβ/ Smads），促丝裂原活化蛋白激酶（MAPKs），高级糖基化终产物（AGEs）以及上皮-间充质转化（EMT）。由于据报导许多炎症介质在鼻息肉（NP）疾病的发展中起着重要作用，这项研究旨在分析AGEs /高级糖基化终产物（RAGE）/细胞外信号调节激酶（ERK）信号通路的受体与EMT的主要标志物之间的相关性，以更好地了解它们对EMT重构的影响。与正常对照相比，受CRSwNP影响的患者的鼻黏膜。本研究共招募了30名患者。使用AGE，RAGE，p-ERK，MMP-3，TGF-β1，Smad2 / 3，I-III胶原，α-SMA，E-钙粘着蛋白，IL-6和波形蛋白抗体进行免疫组织化学分析。还使用蛋白质印迹分析评估了年龄，愤怒，ERK，p-ERK和MMP3。我们观察到CRSwNP与对照组相比，AGE / RAGE / p-ERK和EMT的主要间充质标记物（Vimentin和IL-6）过度表达，而TGF-β/ Smad3通路在两组之间没有显着差异。耐心。这些观察结果表明，NP发病机理是复杂的过程网络，AGE / RAGE / ERK途径和EMT可能在促进CRSwNP形成中的组织重塑中协同作用。