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首页> 外文期刊>Pharmacogenetics and genomics >Protein tyrosine kinase 2beta as a candidate gene for hypertension.
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Protein tyrosine kinase 2beta as a candidate gene for hypertension.

机译：蛋白酪氨酸激酶2beta作为高血压的候选基因。

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Protein tyrosine kinase 2beta (PTK2B) is a member of the focal adhesion kinase family and is activated by angiotensin II through Ca2+-dependent pathways. An evidence exists that PTK2B is involved in cell growth, vascular contraction, inflammatory responses, and salt and water retention through activation of the angiotensin II type 1 receptor. To examine the contribution of PTK2B, we sequenced the PTK2B gene using 48 patients with hypertension, identified 62 genetic polymorphisms, and genotyped six representative single nucleotide polymorphisms in population-based case-control samples from 3655 Japanese individuals (1520 patients with hypertension and 2135 controls). Multivariate logistic regression analysis after adjustments for age, body mass index, present illness (hyperlipidemia and diabetes mellitus), and lifestyle (smoking and drinking) showed -22A>G to have an association with hypertension in men (AA vs. AG+GG: odds ratio=1.27; 95% confidence interval: 1.02-1.57; P=0.030). Another polymorphism, 53484A>C (K838T), in linkage disequilibrium with -22A>G showed a marginal association with hypertension in men (AA vs. AC+CC: odds ratio=1.25; 95% confidence interval: 0.99-1.57; P=0.059). Diastolic blood pressure was 1.6 mmHg higher in men with the AC+CC genotype of 53484A>C than those with the AA genotype (P=0.003), after adjustments for the same factors. These polymorphisms are in linkage disequilibrium with others in a range of 113 kb in PTK2B. The intracellular distribution of the recombinant PTK2B protein and that of the mutant protein with T838 were indistinguishable even after angiotensin II stimulation, both proteins localizing at a focal point in the peripheral area in the cells. Thus, a haplotype in PTK2B may play a role in essential hypertension in Japanese.
机译：蛋白质酪氨酸激酶2beta（PTK2B）是粘着斑激酶家族的成员，并被血管紧张素II通过Ca2 +依赖性途径激活。有证据表明，PTK2B通过激活血管紧张素II 1型受体参与细胞生长，血管收缩，炎症反应以及盐和水保留。为了检查PTK2B的贡献，我们使用48例高血压患者对PTK2B基因进行了测序，确定了62个遗传多态性，并从3655名日本人（1520例高血压患者和2135例对照患者）的人群病例对照样本中对六个代表性的单核苷酸多态性进行了基因分型）。调整年龄，体重指数，当前疾病（高脂血症和糖尿病）和生活方式（吸烟和饮酒）后的多因素logistic回归分析显示，-22A> G与男性高血压相关（AA与AG + GG：比值比= 1.27; 95％置信区间：1.02-1.57; P = 0.030）。连锁不平衡与-22A> G的另一种多态性53484A> C（K838T）显示与男性高血压的边缘相关性（AA vs. AC + CC：优势比= 1.25; 95％置信区间：0.99-1.57; P = 0.059）。在调整了相同因素后，AC + CC基因型为53484A> C的男性的舒张压比AA基因型的男性高1.6 mmHg（P = 0.003）。这些多态性在PTK2B中与其他连锁不平衡，范围为113 kb。即使在血管紧张素II刺激后，重组PTK2B蛋白的细胞内分布和带有T838的突变蛋白的细胞内分布也无法区分，这两种蛋白均位于细胞外围区域的焦点处。因此，PTK2B中的单倍型可能在日本人的原发性高血压中起作用。

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