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前列腺素内过氧化物合酶基因 COX1 和 COX2 - 囊性纤维化患者疾病严重程度的新调节剂。

Prostaglandin-endoperoxide synthase genes COX1 and COX2 - novel modifiers of disease severity in cystic fibrosis patients.

机构信息

Institute of Mother and Child, Department of Medical Genetics, Kasprzaka 17a, 01-211 Warsaw, Poland.

出版信息

J Appl Genet. 2010;51(3):323-30. doi: 10.1007/BF03208862.

Abstract

Cystic fibrosis (CF) is one of the most common autosomal recessive diseases among Caucasians caused by a mutation in the CFTR gene. However, the clinical outcome of CF pulmonary disease varies remarkably even in patients with the same CFTR genotype. This has led to a search for genetic modifiers located outside the CFTR gene. The aim of this study was to evaluate the effect of functional variants in prostaglandin-endoperoxide synthase genes (COX1 and COX2) on the severity of lung disease in CF patients. To the best of our knowledge, it is the first time when analysis of COX1 and COX2 as potential CF modifiers is provided. The study included 94 CF patients homozygous for F508del mutation of CFTR. To compare their clinical condition, several parameters were recorded, e.g. a unique clinical score: disease severity status (DSS). To analyse the effect of non-CFTR genetic polymorphisms on the clinical course of CF patients, the whole coding region of COX1 and selected COX2 polymorphisms were analysed. Statistical analysis of genotype-phenotype associations revealed a relationship between the heterozygosity status of identified polymorphisms and better lung function. These results mainly concern COX2 polymorphisms: -765G>C and 8473T>C. The COX1 and COX2 polymorphisms reducing COX protein levels had a positive effect on all analysed clinical parameters. This suggests an important role of these genes as protective modifiers of pulmonary disease in CF patients, due to inhibition of arachidonic acid conversion into prostaglandins, which probably reduces the inflammatory process.

摘要

囊性纤维化(CF)是最常见的常染色体隐性疾病之一,在白种人中由 CFTR 基因突变引起。然而,即使在具有相同 CFTR 基因型的患者中,CF 肺部疾病的临床结果也有很大差异。这导致了对位于 CFTR 基因之外的遗传修饰物的寻找。本研究旨在评估前列腺素内过氧化物合酶基因(COX1 和 COX2)的功能变体对 CF 患者肺部疾病严重程度的影响。据我们所知,这是首次分析 COX1 和 COX2 作为潜在 CF 修饰物的作用。该研究包括 94 名 CF 患者,他们均为 CFTR 基因 F508del 突变的纯合子。为了比较他们的临床状况,记录了几个参数,例如独特的临床评分:疾病严重程度状态(DSS)。为了分析非 CFTR 遗传多态性对 CF 患者临床过程的影响,分析了 COX1 的整个编码区和选定的 COX2 多态性。基因型-表型关联的统计分析显示,鉴定的多态性的杂合状态与更好的肺功能之间存在关系。这些结果主要涉及 COX2 多态性:-765G>C 和 8473T>C。降低 COX 蛋白水平的 COX1 和 COX2 多态性对所有分析的临床参数均有积极影响。这表明这些基因作为 CF 患者肺部疾病的保护性修饰物具有重要作用,因为它们抑制了花生四烯酸转化为前列腺素,这可能减少了炎症过程。

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