Nature:胎儿视觉的发育依赖于母亲的光照

2013-01-23 Nature dxy shamowenquan

  眼睛不仅依赖光照来视物。近期nature上的新发现表明,孕期(胎儿)眼睛的正常发育同样需要光照(的帮助)。2013年1月16日新一期的《自然》发表了——视觉发生依靠光线——一般来说在孕期视觉的发育也依靠光线。科学家们称,这一意外的发现为胎儿眼发育,以及血管性眼病,尤其对一种称作早产儿视网膜病变的眼病,提供了一些新的基本认识——特别值得一提的是早产儿视网膜病变能引起失明。该研究由辛辛那提州儿童医


  眼睛不仅依赖光照来视物。近期nature上的新发现表明,孕期(胎儿)眼睛的正常发育同样需要光照(的帮助)。2013年1月16日新一期的《自然》发表了——视觉发生依靠光线——一般来说在孕期视觉的发育也依靠光线。科学家们称,这一意外的发现为胎儿眼发育,以及血管性眼病,尤其对一种称作早产儿视网膜病变的眼病,提供了一些新的基本认识——特别值得一提的是早产儿视网膜病变能引起失明。该研究由辛辛那提州儿童医院内科中心和圣弗朗西科加利福利亚大学的科学家牵头,早于1月16日印刷(刊物)出版之前,已在线发布。

  “这份研究这从根本上改变了我们对于视网膜形成机制的理解”,辛辛那提州儿童医院内科中心的小儿眼科学博士、该研究的共同作者Richard Lang说道。我们已能识别控制视网膜神经元数量的光应答通路。这会对眼中的发育血管产生下游影响,由于几种主要的眼疾病都是血管疾病,因此其具有重要的意义。”Lang是该项目的主要研究员,与圣弗朗西科加利福利亚大学眼科学和生理学的科学家DavidCopenhagen博士,将共同进行该项目研究。科学家们表示,在当前的研究中他们利用小鼠模型获得了一些意外的研究发现。

  “小鼠出生后,眼睛发育要经历几个阶段”,Copenhagen说道。“因此,我们常持有这种假设——如果光对眼睛发育起作用,它只该发生于出生之后”。但是研究者在当前的研究中发现在妊娠期间,新描述的那种光反应通路必须得到激活,进而启动精心编排的程序,才能确保生成健康的眼睛。具体来说,到妊娠后期,或是小鼠妊娠约16天时,有足量的光子进入母体非常重要。研究者们也惊奇地发现光子在胎儿(眼里)——而非其母亲——激活了一种叫做黑视素的蛋白质,该蛋白质能帮助眼内的血管和视网膜神经元正常的发育。

  光应答通路其中之一的用途就是抑制视网膜中形成的血管数量(抑制大量血管在视网膜上形成)。这些血管对于视网膜上的神经元非常重要,供给视细胞需要大量的氧气助其(完善)形态和功能。当视网膜病变在早产儿发生时,视网膜血管生长几乎不受控制。这种持续的血管扩展对眼睛发育有强烈的压迫作用,在极端的情况下会引起严重的损伤甚至失明。由Lang andCopenhagen领导的研究小组在实验小鼠模型上进行了几组实验,以此鉴定光应答通路奇特的构成与功能。这些小鼠从妊娠后期开始分别被饲养于黑暗之中,或是按正常昼夜周期饲养,从而比较观察血管发育对眼睛的作用。这些研究者已经通过突变小鼠中的一种称作Opn4的视蛋白基因(生成melanopsin),实质上防止光色素激活,研究人员检验了这一光反应信号的功能

  妊娠后期饲养在黑暗环境中的和有Opn4突变基因的小鼠,呈现出几乎完全一致的玻璃体血管杂乱扩张,以及异常的视网膜血管生长。这些未加抑制的血管生成是受叫做血管内皮因子(Vegfa)的蛋白质驱动的。根据研究者说道,当光应答通路在适当地运作时,它能调制着(血管内皮因子)Vegfa以此来阻止杂乱无章的血管生长。在小鼠与人类妊娠期都有黑视素蛋白质的存在。Lang说道,研究小组正在继续研究这一光反应信号有可能影响早产儿视网膜病以及其他眼疾病易感性的机制。


A direct and melanopsin-dependent fetal light response regulates mouse eye development

Vascular patterning is critical for organ function. In the eye, there is simultaneous regression of embryonic hyaloid vasculature1 (important to clear the optical path) and formation of the retinal vasculature2 (important for the high metabolic demands of retinal neurons). These events occur postnatally in the mouse. Here we have identified a light-response pathway that regulates both processes. We show that when mice are mutated in the gene (Opn4) for the atypical opsin melanopsin345, or are dark-reared from late gestation, the hyaloid vessels are persistent at 8days post-partum and the retinal vasculature overgrows. We provide evidence that these vascular anomalies are explained by a light-response pathway that suppresses retinal neuron number, limits hypoxia and, as a consequence, holds local expression of vascular endothelial growth factor (VEGFA) in check. We also show that the light response for this pathway occurs in late gestation at about embryonic day 16 and requires the photopigment in the fetus and not the mother. Measurements show that visceral cavity photon flux is probably sufficient to activate melanopsin-expressing retinal ganglion cells in the mouse fetus. These data thus show that light—the stimulus for function of the mature eye—is also critical in preparing the eye for vision by regulating retinal neuron number and initiating a series of events that ultimately pattern the ocular blood vessels.
    

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    2013-05-09 liye789132251
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    2013-01-25 neurowu
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    2013-01-25 TZF0807

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