Nature:胎盘对于胎儿健康发育的作用被严重低估!
2018/03/19
胎盘是维持正常妊娠的重要器官,但是它对妊娠并发症、出生缺陷的潜在影响一直被人们所忽视。3月14日,《Nature》期刊最新发表一篇文章揭示,胎盘对于胎儿健康发育的作用被严重低估。


这一研究是究是Wellcome基金会资助的“破译发育缺陷机制”项目(DMDD)的一部分,由Babraham研究所的Myriam Hemberger团队与Sanger研究所、Francis Crick研究所、牛津大学和奥地利维也纳医科大学的科学家们合作完成。

已有的大规模表型研究表明,约25-30%的基因缺失会导致小鼠胎死腹中。但这其中,多少基因突变会影响胎盘呢?

Myriam Hemberger带领团队分析了103个胚胎致死(embryonic lethal)基因,发现胚胎死亡多与胎盘缺陷有直接关联。他们推测,导致胎儿死亡的大量遗传缺陷可能是由于胎盘出现异常,而不是胚胎本身。


doi:10.1038/nature26002

文章作者Vicente Perez-Garcia博士表示:“对于胚胎致死基因的分析多集中于胚胎,而不是胎盘。现在最新研究提醒我们,致死基因引发胎盘缺陷远比想象的要严重。有意思的是,胎盘发生问题的组织多位于胚胎本身缺陷的旁边。”

结果显示,68%的胚胎致死基因突变会在妊娠中后期表现出胎盘畸形。而且,怀孕初期的死亡几乎都与胎盘缺陷有关。研究人员发现,胎盘缺陷与胎儿大脑、心脏和血管异常发育有关。

虽然这份研究使用的是小鼠模型,但是它依然对于人类怀孕期间的并发症有很大的指示意义,强调了胎盘对于胎儿健康发育的重要性。

参考资料:

Alomst 70 percent of 103 genes linked to prenatal death affect the placenta

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  • Placentation defects are highly prevalent in embryonic lethal mouse mutants

    Large-scale phenotyping efforts have demonstrated that approximately 25–30% of mouse gene knockouts cause intrauterine lethality. Analysis of these mutants has largely focused on the embryo and not the placenta, despite the crucial role of this extraembryonic organ for developmental progression. Here we screened 103 embryonic lethal and sub-viable mouse knockout lines from the Deciphering the Mechanisms of Developmental Disorders program for placental phenotypes. We found that 68% of knockout lines that are lethal at or after mid-gestation exhibited placental dysmorphologies. Early lethality (embryonic days 9.5–14.5) is almost always associated with severe placental malformations. Placental defects correlate strongly with abnormal brain, heart and vascular development. Analysis of mutant trophoblast stem cells and conditional knockouts suggests that a considerable number of factors that cause embryonic lethality when ablated have primary gene function in trophoblast cells. Our data highlight the hugely under-appreciated importance of placental defects in contributing to abnormal embryo development and suggest key molecular nodes that govern placenta formation.

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