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本文引用的文献

1
Uterine natural killer cells initiate spiral artery remodeling in human pregnancy.子宫自然杀伤细胞启动人类妊娠中的螺旋动脉重塑。
FASEB J. 2012 Dec;26(12):4876-85. doi: 10.1096/fj.12-210310. Epub 2012 Aug 23.
2
Placental histopathological findings in obese and nonobese women with complicated and uncomplicated pregnancies.肥胖和非肥胖孕妇中合并症和非合并症妊娠的胎盘组织病理学发现。
Arch Gynecol Obstet. 2012 Dec;286(6):1343-7. doi: 10.1007/s00404-012-2450-z. Epub 2012 Jul 14.
3
Regulatory pathways controlling the endovascular invasive trophoblast cell lineage.调控血管内侵袭性滋养层细胞谱系的信号通路。
J Reprod Dev. 2012;58(3):283-7. doi: 10.1262/jrd.2011-039.
4
Biological mechanisms for nutritional regulation of maternal health and fetal development.营养调节母婴健康和胎儿发育的生物学机制。
Paediatr Perinat Epidemiol. 2012 Jul;26 Suppl 1:4-26. doi: 10.1111/j.1365-3016.2012.01291.x.
5
Impaired decidual natural killer cell regulation of vascular remodelling in early human pregnancies with high uterine artery resistance.在高子宫动脉阻力的早期人类妊娠中,蜕膜自然杀伤细胞对血管重塑的调节受损。
J Pathol. 2012 Nov;228(3):322-32. doi: 10.1002/path.4057. Epub 2012 Jul 18.
6
Extravillous trophoblast and decidual natural killer cells: a remodelling partnership.绒毛外滋养细胞和蜕膜自然杀伤细胞:重塑伴侣关系。
Hum Reprod Update. 2012 Jul;18(4):458-71. doi: 10.1093/humupd/dms015. Epub 2012 Apr 20.
7
The role of vascular smooth muscle cell apoptosis and migration during uterine spiral artery remodeling in normal human pregnancy.正常妊娠中子宫螺旋动脉重塑过程中血管平滑肌细胞凋亡和迁移的作用。
FASEB J. 2012 Jul;26(7):2975-85. doi: 10.1096/fj.12-203679. Epub 2012 Apr 12.
8
Adverse fetal and neonatal outcomes associated with a life-long high fat diet: role of altered development of the placental vasculature.长期高脂肪饮食与胎儿和新生儿不良结局相关:胎盘血管发育改变的作用。
PLoS One. 2012;7(3):e33370. doi: 10.1371/journal.pone.0033370. Epub 2012 Mar 19.
9
Maternal resveratrol treatment during pregnancy improves adverse fetal outcomes in a rat model of severe hypoxia.孕期给予母体白藜芦醇治疗可改善严重缺氧大鼠模型的不良胎儿结局。
Placenta. 2012 May;33(5):449-52. doi: 10.1016/j.placenta.2012.01.012. Epub 2012 Feb 10.
10
Rat placentation: an experimental model for investigating the hemochorial maternal-fetal interface.大鼠胎盘形成:研究合胞体母体-胎儿界面的实验模型。
Placenta. 2012 Apr;33(4):233-43. doi: 10.1016/j.placenta.2011.11.026. Epub 2012 Jan 28.

在终身母体肥胖的大鼠模型中,滋养细胞浸润和血管重塑发生改变。

Trophoblast invasion and blood vessel remodeling are altered in a rat model of lifelong maternal obesity.

机构信息

1Department of Pediatrics and the Graduate Program in Medical Sciences, McMaster University, Hamilton, Ontario, Canada.

出版信息

Reprod Sci. 2014 May;21(5):648-57. doi: 10.1177/1933719113508815. Epub 2013 Oct 23.

DOI:10.1177/1933719113508815
PMID:24155067
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3984483/
Abstract

Maternal obesity is associated with an increased risk of a number of pregnancy complications, including fetal demise, which may be linked to impaired placental development as a result of altered trophoblast invasion and vessel remodeling. Therefore, we examined these parameters in pregnant rats fed a control (normal weight) or high fat (HF) diet (obese) at 2 critical times of rat placental development. Early trophoblast invasion was increased by approximately 2-fold in HF-fed dams with a concomitant increase in the expression of matrix metalloproteinase 9 protein, a mediator of tissue remodeling and invasion. Furthermore, we observed significantly higher levels of smooth muscle actin surrounding the placental spiral arteries of HF-fed dams, suggesting impaired spiral artery remodeling. Taken together, the results of this study suggest that altered placental development is an important contributor to the poor pregnancy outcomes and increased fetal demise in our model of lifelong maternal obesity.

摘要

母体肥胖与许多妊娠并发症的风险增加有关,包括胎儿死亡,这可能与胎盘发育受损有关,因为滋养细胞侵入和血管重塑发生改变。因此,我们在妊娠大鼠中检查了在大鼠胎盘发育的 2 个关键时期给予对照(正常体重)或高脂肪(HF)饮食(肥胖)的这些参数。HF 喂养的母鼠中的早期滋养细胞侵入增加了约 2 倍,伴随着基质金属蛋白酶 9 蛋白表达的增加,基质金属蛋白酶 9 蛋白是组织重塑和侵入的介质。此外,我们观察到 HF 喂养的母鼠胎盘螺旋动脉周围的平滑肌肌动蛋白水平明显升高,表明螺旋动脉重塑受损。总之,这项研究的结果表明,胎盘发育改变是我们终生母体肥胖模型中妊娠结局不良和胎儿死亡增加的重要原因。