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母系微生物组促进小鼠胎盘发育。

The maternal microbiome promotes placental development in mice.

机构信息

Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.

The Shapiro Family Laboratory of Viral Oncology and Aging Research, University of California, Los Angeles, Los Angeles, CA, USA.

出版信息

Sci Adv. 2023 Oct 6;9(40):eadk1887. doi: 10.1126/sciadv.adk1887.

DOI:10.1126/sciadv.adk1887
PMID:37801498
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10558122/
Abstract

The maternal microbiome is an important regulator of gestational health, but how it affects the placenta as the interface between mother and fetus remains unexplored. Here, we show that the maternal gut microbiota supports placental development in mice. Depletion of the maternal gut microbiota restricts placental growth and impairs feto-placental vascularization. The maternal gut microbiota modulates metabolites in the maternal and fetal circulation. Short-chain fatty acids (SCFAs) stimulate cultured endothelial cell tube formation and prevent abnormalities in placental vascularization in microbiota-deficient mice. Furthermore, in a model of maternal malnutrition, gestational supplementation with SCFAs prevents placental growth restriction and vascular insufficiency. These findings highlight the importance of host-microbial symbioses during pregnancy and reveal that the maternal gut microbiome promotes placental growth and vascularization in mice.

摘要

母体微生物组是妊娠健康的重要调节剂,但它如何影响胎盘作为母体和胎儿之间的界面仍未被探索。在这里,我们表明母体肠道微生物群支持小鼠胎盘的发育。母体肠道微生物群的耗竭限制了胎盘的生长并损害了胎-胎盘血管化。母体肠道微生物群调节母体和胎儿循环中的代谢物。短链脂肪酸(SCFAs)刺激培养的内皮细胞管形成,并防止缺乏微生物群的小鼠胎盘血管化异常。此外,在母体营养不良的模型中,SCFAs 的妊娠补充可防止胎盘生长受限和血管功能不全。这些发现强调了怀孕期间宿主-微生物共生的重要性,并揭示了母体肠道微生物群促进了小鼠胎盘的生长和血管化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/d876eedec53b/sciadv.adk1887-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/f77e564319e1/sciadv.adk1887-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/53bf2bddab97/sciadv.adk1887-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/11c70fd03d98/sciadv.adk1887-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/d876eedec53b/sciadv.adk1887-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/f77e564319e1/sciadv.adk1887-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/53bf2bddab97/sciadv.adk1887-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/11c70fd03d98/sciadv.adk1887-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e764/10558122/d876eedec53b/sciadv.adk1887-f4.jpg

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GPR43 regulates sodium butyrate-induced angiogenesis and matrix remodeling.
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Pflugers Arch. 2025 Aug 11. doi: 10.1007/s00424-025-03107-2.
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Proc Natl Acad Sci U S A. 2025 Jul 29;122(30):e2426341122. doi: 10.1073/pnas.2426341122. Epub 2025 Jul 25.
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Feto-placental blood vessel development.胎儿-胎盘血管发育
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