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PLGF，宫内酒精暴露后胎儿脑缺陷的胎盘标志物。

PLGF, a placental marker of fetal brain defects after in utero alcohol exposure.

机构信息

UNIROUEN, Inserm U1245 and Rouen University Hospital, Normandy Centre for Genomic and Personalized Medicine, Normandie University, Rouen, France.

Department of Pathology, Rouen University Hospital, Rouen, France.

出版信息

Acta Neuropathol Commun. 2017 Jun 6;5(1):44. doi: 10.1186/s40478-017-0444-6.

DOI:10.1186/s40478-017-0444-6
PMID:28587682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5461764/
Abstract

Most children with in utero alcohol exposure do not exhibit all features of fetal alcohol syndrome (FAS), and a challenge for clinicians is to make an early diagnosis of fetal alcohol spectrum disorders (FASD) to avoid lost opportunities for care. In brain, correct neurodevelopment requires proper angiogenesis. Since alcohol alters brain angiogenesis and the placenta is a major source of angiogenic factors, we hypothesized that it is involved in alcohol-induced brain vascular defects. In mouse, using in vivo repression and overexpression of PLGF, we investigated the contribution of placenta on fetal brain angiogenesis. In human, we performed a comparative molecular and morphological analysis of brain/placenta angiogenesis in alcohol-exposed fetuses. Results showed that prenatal alcohol exposure impairs placental angiogenesis, reduces PLGF levels and consequently alters fetal brain vasculature. Placental repression of PLGF altered brain VEGF-R1 expression and mimicked alcohol-induced vascular defects in the cortex. Over-expression of placental PGF rescued alcohol effects on fetal brain vessels. In human, alcohol exposure disrupted both placental and brain angiogenesis. PLGF expression was strongly decreased and angiogenesis defects observed in the fetal brain markedly correlated with placental vascular impairments. Placental PGF disruption impairs brain angiogenesis and likely predicts brain disabilities after in utero alcohol exposure. PLGF assay at birth could contribute to the early diagnosis of FASD.

摘要

大多数宫内酒精暴露的儿童并不表现出胎儿酒精谱系障碍（FAS）的所有特征，临床医生面临的挑战是早期诊断胎儿酒精谱系障碍（FASD），以避免错失治疗机会。在大脑中，正确的神经发育需要适当的血管生成。由于酒精会改变大脑的血管生成，而胎盘是血管生成因子的主要来源，我们假设它参与了酒精引起的大脑血管缺陷。在小鼠中，我们使用 PLGF 的体内抑制和过表达来研究胎盘对胎儿大脑血管生成的贡献。在人类中，我们对酒精暴露胎儿的大脑/胎盘血管生成进行了分子和形态学比较分析。结果表明，产前酒精暴露会损害胎盘血管生成，降低 PLGF 水平，从而改变胎儿大脑血管系统。胎盘 PLGF 的抑制改变了大脑 VEGF-R1 的表达，并模拟了皮质中酒精引起的血管缺陷。胎盘 PGF 的过表达挽救了酒精对胎儿大脑血管的影响。在人类中，酒精暴露破坏了胎盘和大脑的血管生成。PLGF 的表达明显降低，胎儿大脑中的血管生成缺陷与胎盘血管损伤明显相关。胎盘 PGF 的破坏会损害大脑血管生成，并可能预测宫内酒精暴露后的大脑残疾。出生时进行 PLGF 检测可能有助于 FASD 的早期诊断。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/43c30cfe27b2/40478_2017_444_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/882986a34f78/40478_2017_444_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/a375414c47d8/40478_2017_444_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/8de4e33cafd4/40478_2017_444_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/f44cadf12dfa/40478_2017_444_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/43c30cfe27b2/40478_2017_444_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/882986a34f78/40478_2017_444_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/1fc977bc6fc5/40478_2017_444_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/4be5a0ea47b7/40478_2017_444_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/a375414c47d8/40478_2017_444_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/8de4e33cafd4/40478_2017_444_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/f44cadf12dfa/40478_2017_444_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fde0/5461764/43c30cfe27b2/40478_2017_444_Fig7_HTML.jpg

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