纤维素结构和功能的遗传调节:复杂的基因环境相互作用可能会调节血管风险
Bernard C B Lim1, Robert A S Ariëns, Angela M Carter
1Academic Unit of Molecular Vascular Medicine, University of Leeds, Leeds, UK.
Lancet (London, England)
|May 3, 2003
概括
纤维素和XIII因子的遗传变异影响纤维素凝块结构. 这些相互作用,以及纤维素素水平,影响动脉瘤风险,解决先前研究的差异.
科学领域:
- 生物化学 生物化学
- 遗传学 是一个遗传学.
- 心血管研究研究心血管研究
背景情况:
- 纤维素素和XIII因子基因中的多态性与动脉血风险有关.
- 临床和实验室研究显示,关于这些关联的发现不一致.
- 以前的研究还没有完全阐明这些观测背后的机制.
研究的目的:
- 为了研究XIII因子和纤维素原基因多态性之间的相互作用.
- 检查纤维素度与纤维素结构/功能之间的关系.
- 澄清这些因素对心血管风险的影响.
主要方法:
- 使用透分析和电子显微镜.
- 研究了纤维素结构,XIII Val34Leu因子和纤维素多态 (Aalpha Thr312Ala,Bbeta Arg448Lys) 之间的相互作用.
- 在等离子体和净化系统中进行了分析.
主要成果:
- 较高的纤维素度与纤维素透性降低相关.
- 与34Leu等位基相比,XIII因子34Val等位基导致纤维素凝块更紧.
- 纤维素原Aalpha 312Ala也影响了纤维素的透性,类似于312Thr.
结论:
- 纤维素和XIII因子中的编码多态性与纤维素度相互作用,改变纤维素的结构和功能.
- 这些相互作用解释了流行病学发现和XIII因子34Leu的体外效应之间的悖论.
- 基因-基因和基因-环境相互作用可能会导致心血管风险复杂性.
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