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Nat Genet:12 万人基因测序找到预防青光眼的突变基因

2017-08-02 佚名 药明康德

青光眼作为当今全球不可逆失明的主要原因,深深的困扰着许多人。近日,一项迄今为止规模最大的青光眼国际研究合作有可能为治疗和预防青光眼指明了方向。这项涉及全世界 6 大洲 36 个国家 12 万多人的研究,用深度基因测序的方法,发现了一种可以预防青光眼的突变基因。这项研究结果最近发表在《自然》子刊《Nature Genetics》期刊上。


▲青光眼是老年人失明的最常见原因,了解发病机制有助于治疗药物研发。(图片来源:A-Star)

青光眼作为当今全球不可逆失明的主要原因,深深的困扰着许多人。近日,一项迄今为止规模最大的青光眼国际研究合作有可能为治疗和预防青光眼指明了方向。这项涉及全世界 6 大洲 36 个国家 12 万多人的研究,用深度基因测序的方法,发现了一种可以预防青光眼的突变基因。这项研究结果最近发表在《自然》子刊《Nature Genetics》期刊上。

剥落性综合症 (Exfoliation syndrome,XFS) 是最常见的继发性青光眼 (Secondary glaucoma) 的原因,也是开角型青光眼 (Open-angle glaucoma) 的预兆,可导致视力障碍和失明。这种年龄相关的眼病,会使眼睛的前部 (虹膜、睫状体、晶状体和小体) 出现异常的白片。XFS 是一种由于组织中过度产生和逐步积累异常的细胞外物质,而形成的细胞外基质 (ECM) 的系统性障碍。这种疾病在许多人群中很常见,据估计全世界范围内,有 6000-7000 万人受感染。剥脱性青光眼 (XFG) 常常需要激光和外科介入治疗,是全球范围内不可逆失明的主要原因。

XFS 患者的家族关联显示基因遗传是发病的主要原因,这一观察也为后来的青光眼研究指出了方向。2007 年冰岛的一份研究发现,一个常见基因 LOXL1 的变体显示出与 XFS 有很紧密的联系。然而,这样一种 LOXL1 遗传标记的关联在不同族群中,却显示出完全相反的结果,因此该变体对健康的影响尚不清楚。在这项最新研究中,新加坡研究人员发现了 LOXL1 基因中罕见的保护性突变。这种 p.Y407F 突变为 XFS 提供了 25 倍的保护,这也是迄今为止在同类常见复杂疾病中所见过的最大程度的保护机制。

LOXL1 是一种编码赖氨酰基氧化酶同系物 1(Lysyl oxidase homolog 1)的基因,是已知的第一个与这种疾病有关的基因位点,在疾病发病机制中被认为起到了核心作用。尽管多态性映射到 LOXL1 的遗传关联有着压倒性的证据,但该等位基因也有几率在某些人群中被“翻转”,使得结果不一致。这种明显的等位基因逆转意味着 XFS 疾病生物学的遗传体系结构是复杂的,值得进一步研究。在 LOXL1 中常见的等位基因翻转不太可能是由于同一族群内的抽样差异,因为已被多个重复试验证实了。研究显示,它们也不可能是由于不同人群的不同的 LD 结构导致的。

对 LOXL1 的深度重新测序使研究人员观察到一种罕见的 p.Tyr407Phe 变异。该研究证实了这种罕见的 p.Tyr407Phe 等位基因的功能和生理作用,它对 XPS 具有很强的保护作用,甚至使其自身超越了基因组的重要性。p.Tyr407Phe 替代了位于 LOXL1 的进化上高度保守的催化区。后续的生物实验表明,保护作用可能是由于弹性蛋白和纤维蛋白 - 1 沉积的增加而使 ECM 稳定的结果。


▲研究涉及的 LOXL1 蛋白质突变位置

这一概念得到了组织病理学实验的支持,该实验显示了在 XFS 患者的眼部组织中,它可以降低弹性纤维的形成和组织刚度,以及受损的细胞粘连。研究人员推测,携带这种稀有的保护性的 p.Tyr407Phe 变异可以维持细胞的完整性,使细胞更能抵抗破坏 ECM 的环境压力。研究人员同时也小心的指出,这种方法的一个局限性是 p.Tyr407Phe 的生物机制没有在 RNA 层面上进行测试,因为有可能 p.Tyr407Phe 会影响 RNA 的稳定性。从全基因组关联分析(GWAS)中出现的 7 个位点并不影响单一的发病途径,这也支持了 XFS 是一种复杂的系统性的老化疾病,可能由多种途径和不同类型组织的遗传病变引起的假设。

在这项研究中,研究人员发现除了 POMP 和 TMEM136 外,还有 3 个 XFS 易感基因位点,它映射到 Class III MHC 区域的 AGPAT1(6p21),到 RBMS3(3p24)和接近 SEMA6A(5q23)。AGPAT1 被确定为ω- 6(n - 6)多不饱和脂肪酸 (PUFA) 水平的易感位点,这可能与老龄化人口中的心血管风险有关。据报道,MHC 位点 (AGPAT1 所在位置) 也与阿兹海默症和帕金森病直接相关,它们与 XFS 一样是与年龄相关的疾病。尽管 AGPAT1、RBMS3 和 SEMA6A 的生物学作用还没有被完全了解,但这些位点关联上的一致证据为研究 XFS 疾病的生物学机制提供了进一步的途径。

该研究的通讯作者之一、GIS 的人类遗传学首席研究员 Khor Chiea Chuen 博士解释说:“自然发生的基因变异是很难找到的,但一旦发现,它们就会精确的指出潜在的药物靶点。这就是我们所说的‘自然的意外和实验’。LOXL1 的 p.Y407F 的罕见变异就是这样的一个例子。”


▲论文的第一作者 Aung Tin 教授(图片来源:新加坡国立大学)

论文的第一作者,SERI 的执行主任、SNEC 的副医学主任 Aung Tin 教授说: “这是有史以来最大的青光眼遗传学研究,由来自 35 个其他国家的医学中心和病人共同参与, 这项研究的协调工作非常具有挑战性,而主要工作都在新加坡完成。这些发现非常令人兴奋,因为它能指引治疗青光眼的新疗法。”

文章的共同通讯作者,哈佛医学院 (Harvard Medical School) 的眼科学教授 Janey L. Wiggs 博士说:“这些结果提高了我们对青光眼的认识,也为这一常见的致盲疾病指出了重要的治疗策略。”

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    2017-12-07 liye789132251
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    2018-06-27 canlab
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    2017-08-31 cy0324
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    2017-08-02 hhh678

    henhao

    0

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    2017-08-02 三生有幸9135

    学习一下谢谢分享

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    2017-08-02 1dd8c52fm63(暂无匿称)

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    2017-08-02 1ddf0692m34(暂无匿称)

    学习了,值得分享

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