Decreased CFTR/PPARgamma and increased transglutaminase 2 in nasal polyps

Decreased CFTR/PPARgamma and increased transglutaminase 2 in nasal polyps
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鼻息肉中 CFTR/PPARgamma 降低和转谷氨酰胺酶 2 升高

DOI:
10.1016/j.anl.2021.10.006
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发表时间:
2022
期刊:
影响因子:
1.7
通讯作者:
Kitamura T
Kitamura T
中科院分区:
医学3区
文献类型:
--
作者:
Nguyen TN;Suzuki H;Yoshida Y;Ohkubo J-I;Wakasugi T;Kitamura T

文献摘要

相似文献

转氨酶(TGM)2和过氧化物酶体增殖物激活受体(PPAR)γ被认为参与囊性纤维化(CF)鼻息肉形成的发病机制。我们研究了囊性纤维化跨膜传导调节因子(CFTR)、TGM 2、PPARγ和TGM反应产物异肽键在非CF鼻息肉中的表达。荧光免疫组化和定量RT-PCR检测CFTR、TGM 2、异肽键和PPARγ的表达。结果鼻息肉组织中CFTR和PPARγ的免疫组化荧光强度显著低于鼻甲黏膜,而TGM 2和异肽键的免疫组化荧光强度显著高于鼻甲黏膜。免疫印迹法检测CFTR在鼻息肉中的表达低于在鼻甲黏膜中的表达。PPARGmRNA在鼻息肉中的表达明显低于鼻甲黏膜,而CFTRmRNA和TGM 2 mRNA在两种组织中的表达无差异。CFTR与TGM 2、异肽键呈显著负相关,与PPARγ呈显著正相关。TGM 2的荧光强度与异肽键的荧光强度呈正相关,与PPARγ的荧光强度呈负相关。结论CFTR-TGM 2-PPARγ级联反应在非CF患者鼻息肉形成中可能起着与CF患者相同的作用。
ObjectiveTransglutaminase (TGM)2 and peroxisome proliferator-activated receptor (PPAR)γ are thought to participate in the pathogenesis of nasal polyp formation in cystic fibrosis (CF). We herein investigated expressions of cystic fibrosis transmembrane conductance regulator (CFTR), TGM2, PPARγ and isopeptide bonds, a reaction product of TGM, in non-CF nasal polyps.MethodsNasal polyps and inferior turbinates were collected from chronic rhinosinusitis patients without CF during transnasal endoscopic sinonasal surgery. Expressions of CFTR, TGM2, isopeptide bonds and PPARγ were examined by fluorescence immunohistochemistry and quantitative RT-PCR. Expression of CFTR was also analyzed by Western blot.ResultsImmunohistochemical fluorescence of the nasal polyp was significantly lower for CFTR and PPARγ, and significantly higher for TGM2 and isopeptide bonds than that of the turbinate mucosa. Lower expression of CFTR in the nasal polyp than in the turbinate mucosa was also observed in Western blot. Expression ofPPARGmRNA was significantly lower in the nasal polyp than in the turbinate mucosa, whereas expressions ofCFTRmRNA orTGM2mRNA did not differ between the two tissues. Immunohistochemical fluorescence for CFTR showed significant negative correlation with that for TGM2 and isopeptide bonds, and significant positive correlation with that for PPARγ. The fluorescence for TGM2 was positively correlated with that for isopeptide bonds and negatively correlated with that for PPARγ. The fluorescence for isopeptide bonds tended to be negatively correlated with that for PPARγ.ConclusionsThese results suggest a possible role of the CFTR-TGM2-PPARγ cascade in the pathogenesis of nasal polyp formation in non-CF patients as in CF patients.