Suppr超能文献

伊朗可能患有家族性高胆固醇血症患者的分子特征分析

Molecular characterization of Iranian patients with possible familial hypercholesterolemia.

作者信息

Farrokhi E, Shayesteh F, Asadi Mobarakeh S, Roghani Dehkordi F, Ghatreh Samani K, Hashemzadeh Chaleshtori M

出版信息

Indian J Clin Biochem. 2011 Jul;26(3):244-8. doi: 10.1007/s12291-011-0113-7. Epub 2011 Feb 10.

Abstract

Familial hypercholesterolemia (FH) is an autosomal dominant disorder of lipoprotein metabolism caused mainly by mutations in the low-density lipoprotein receptor (LDLR) and apolipoprotein B 100 (APOB) genes. Until now, the molecular basis of FH has been demonstrated in detail in many populations, but there is still very limited Molecular data concerning FH in Iran. The aim of this study was to characterize the LDLR and APOB gene mutations in an Iranian population. A total of 30 non-related Iranian possible FH subjects were studied. Diagnosis of FH was based on the Dutch Lipid Clinic Network diagnostic criteria. All samples were initially tested for three common APOB gene mutations including R3500Q, R3500 W and R3531C using PCR-RFLP assay. Subsequently, promoter and coding region of the LDLR gene was screened by PCR-SSCP analysis and positive results were confirmed by DNA sequencing. Four previously reported polymorphisms 1413G > A, 1725C > T, 1773T > C and 2140 + 5G > A were found in ~17% (5/30) of population studied. Moreover, no variation was found in APOB gene. Our data indicated that LDLR and APOB gene mutations have not contribution to possible FH in Iranian population studied here. However, we examined three common APOB mutations and LDLR in only 30 patients, and to determine the role of these genes in developing FH in Iran, more FH samples and populations needed to be investigated for the mutations of the related genes.

摘要

家族性高胆固醇血症(FH)是一种常染色体显性脂蛋白代谢紊乱疾病,主要由低密度脂蛋白受体(LDLR)和载脂蛋白B 100(APOB)基因突变引起。到目前为止,FH的分子基础在许多人群中已得到详细证实,但关于伊朗FH的分子数据仍然非常有限。本研究的目的是鉴定伊朗人群中LDLR和APOB基因突变情况。共研究了30名无亲缘关系的可能患有FH的伊朗受试者。FH的诊断基于荷兰脂质诊所网络诊断标准。所有样本首先使用PCR-RFLP分析法检测三种常见的APOB基因突变,包括R3500Q、R3500W和R3531C。随后,通过PCR-SSCP分析筛查LDLR基因的启动子和编码区,并通过DNA测序确认阳性结果。在约17%(5/30)的研究人群中发现了四个先前报道的多态性位点1413G>A、1725C>T、1773T>C和2140+5G>A。此外,在APOB基因中未发现变异。我们的数据表明,LDLR和APOB基因突变对本研究中的伊朗人群可能患有的FH没有影响。然而,我们仅在30名患者中检测了三种常见的APOB突变和LDLR,为确定这些基因在伊朗FH发病中的作用,需要对更多的FH样本和人群进行相关基因突变的研究。

相似文献

8
Familial defective apolipoprotein B-100: A review.家族性载脂蛋白B-100缺陷:综述
J Clin Lipidol. 2016 Nov-Dec;10(6):1297-1302. doi: 10.1016/j.jacl.2016.09.009. Epub 2016 Sep 22.

引用本文的文献

本文引用的文献

5
The mutation APOB-100 R3500Q in Eastern Europe.东欧的载脂蛋白B-100 R3500Q突变。
Atherosclerosis. 2001 May;156(1):241-2. doi: 10.1016/s0021-9150(01)00482-8.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验