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首页> 外文期刊>Genomics >Epistatic effects of polymorphisms in genes from the renin-angiotensin, bradykinin, and fibrinolytic systems on plasma t-PA and PAI-1 levels.
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Epistatic effects of polymorphisms in genes from the renin-angiotensin, bradykinin, and fibrinolytic systems on plasma t-PA and PAI-1 levels.

机译：肾素-血管紧张素，缓激肽和纤溶系统基因多态性对血浆t-PA和PAI-1水平的上位作用。

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摘要

Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) directly influence thrombus formation and degradation and thereby risk for arterial thrombosis. Activation of the renin-angiotensin system has been linked to the production of PAI-1 expression via the angiotensin II type 1 receptor (AT1R). In addition, bradykinin can induce the release of t-PA through a B2 receptor mechanism. In the present study, we aimed to investigate the epistatic effects of polymorphisms in genes from the renin-angiotensin, bradykinin, and fibrinolytic systems on plasma t-PA and PAI-1 levels in a large population-based sample (n=2527). We demonstrated a strong significant interaction within genetic variations of the bradykinin B2 gene (P=0.002) and between ACE and bradykinin B2 (p=0.003) polymorphisms on t-PA levels in females. In males, polymorphisms in the bradykinin B2 and AT1R gene showed the most strong effect on t-PA levels (P=0.006). In both females and males, the bradykinin B2 gene interactedwith AT1R gene on plasma PAI-1 levels (P=0.026 and P=0.039, respectively). In addition, the current study found a borderline significant interaction between PAI 4G5G and ACE I/D on plasma t-PA and PAI-1 levels. These results support the idea that the interplay between the renin-angiotensin, bradykinin, and fibrinolytic systems might play an important role in t-PA and PAI-1 biology.
机译：组织纤溶酶原激活物（t-PA）和纤溶酶原激活物抑制剂1（PAI-1）直接影响血栓的形成和降解，从而影响动脉血栓形成的风险。肾素-血管紧张素系统的激活通过血管紧张素II 1型受体（AT1R）与PAI-1表达的产生有关。另外，缓激肽可通过B2受体机制诱导t-PA的释放。在本研究中，我们旨在研究大样本人群（n = 2527）中肾素-血管紧张素，缓激肽和纤溶系统基因多态性对血浆t-PA和PAI-1水平的影响。我们证明了女性缓激肽B2基因的遗传变异（P = 0.002）以及ACE和缓激肽B2的多态性（p = 0.003）之间在女性t-PA水平上有很强的显着相互作用。在男性中，缓激肽B2和AT1R基因的多态性对t-PA水平的影响最大（P = 0.006）。在雌性和雄性中，缓激肽B2基因都与AT1R基因在血浆PAI-1水平上相互作用（分别为P = 0.026和P = 0.039）。此外，当前的研究发现PAI 4G5G与ACE I / D在血浆t-PA和PAI-1水平上具有临界的显着相互作用。这些结果支持以下观点：肾素-血管紧张素，缓激肽和纤溶系统之间的相互作用可能在t-PA和PAI-1生物学中起重要作用。

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