Department of Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
Hypertension. 2013 Jul;62(1):41-7. doi: 10.1161/HYPERTENSIONAHA.113.01330. Epub 2013 May 6.
The angiotensinogen gene is genetically linked with hypertension, but the mechanistic basis for association of sequence variants in the promoter and coding region of the gene remains unclear. An E-box at position -20 has been hypothesized to control the level of angiotensinogen expression, but its mechanistic importance for angiotensinogen expression in human tissues is uncertain. We developed an allele-specific polymerase chain reaction-based assay to distinguish between angiotensinogen mRNA derived from variants at the -20 position (rs5050) in the angiotensinogen promoter in adipose tissues obtained during surgery. The assay takes advantage of linkage disequilibrium between the rs5050 (located in the promoter) and rs4762 (located in the coding region) single nucleotide polymorphisms. This strategy allowed us to assess the level of allele-specific expression in A-20C heterozygous subjects comparing the relative proportion of each allele with the total, thus eliminating the problem of variability in the level of total angiotensinogen mRNA among subjects. We show that angiotensinogen mRNA derived from the -20C allele is expressed significantly higher than that derived from the -20A allele in subcutaneous adipose tissue, and increased expression correlates with enriched chromatin binding of upstream stimulatory factor-2 to the -20C E-box compared with -20A. This may be depot selective because we were unable to detect these differences in omental adipose. This provides the first data directly comparing expression of angiotensinogen mRNA and differential transcription factor binding derived from 2 variant alleles in human tissue where the ratio of expression of one allele to another can be accurately determined.
血管紧张素原基因与高血压在遗传学上有关联,但基因启动子和编码区序列变异与高血压相关联的机制基础仍不清楚。有人假设-20 位置的 E 盒可控制血管紧张素原表达水平,但它对人类组织中血管紧张素原表达的机制重要性尚不确定。我们开发了一种等位基因特异性聚合酶链反应(PCR)检测方法,以区分在手术中获得的脂肪组织中血管紧张素原启动子的-20 位(rs5050)的等位基因特异性血管紧张素原 mRNA。该检测方法利用 rs5050(位于启动子)和 rs4762(位于编码区)单核苷酸多态性之间的连锁不平衡。该策略使我们能够评估 A-20C 杂合子个体中等位基因特异性表达的水平,比较每个等位基因与总基因的相对比例,从而消除了个体间总血管紧张素原 mRNA 水平变化的问题。我们发现,来源于 -20C 等位基因的血管紧张素原 mRNA 在皮下脂肪组织中的表达明显高于来源于 -20A 等位基因的表达,并且表达增加与上游刺激因子-2 与 -20C E 盒的富集染色质结合相关,而与 -20A 则无相关。这可能是脂肪组织特异性的,因为我们无法在网膜脂肪组织中检测到这些差异。这首次提供了在可以准确确定一个等位基因表达与另一个等位基因表达比例的人类组织中,直接比较血管紧张素原 mRNA 的表达和差异转录因子结合的来自 2 个变异等位基因的表达的数据。