The influence of the intrauterine environment on human placental development
Abstract
Development of the human placenta is modulated heavily by the intrauterine environment. During the first trimester, development takes place in a low oxygen environment supported by histiotrophic nutrition from the endometrial glands. Consequently, the rate of growth of the chorionic sac is almost invariable across this period, and is remarkably uniform between individuals. Towards the end of the first trimester the intrauterine environment undergoes radical transformation in association with onset of the maternal arterial circulation and the switch to haemotrophic nutrition. The accompanying rise in intraplacental oxygen concentration poses a major challenge to placental tissues, and extensive villous remodelling takes place at this time. Later in pregnancy a wide variety of stressors are capable of affecting placental growth, but in the human, the most common are nutrient deprivation and vascular compromise. The latter is usually secondary to deficient trophoblast invasion and can induce placental oxidative stress. Closely linked to oxidative stress is endoplasmic reticulum stress, and we recently provided the first evidence that the latter plays a major role in the pathophysiology of intrauterine growth restriction. The endoplasmic reticulum is a key regulator of protein synthesis, exerting its effects through the unfolded protein response. Consequently, we observed multiple blocks to translation initiation and elongation in growth restricted placentas. Nutrient deprivation also modulates protein synthesis through the mTOR pathway, and we demonstrated interactions between this pathway and endoplasmic reticulum stress. Protein synthesis inhibition therefore appears to be a common mechanism for regulating placental development under different adverse conditions.
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Excessive villous regression at the time of onset of the maternal circulation may indicate deficient extravillous trophoblast invasion, which may mean that the remaining spiral arteries are not fully remodeled, compromising placental blood flow.
“For the latter, excessive villous regression at the time of onset of the maternal circulation may be indicative of deficient extravillous trophoblast invasion (77), which may mean that the remaining spiral arteries are not fully remodeled, compromising placental blood flow.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [77]
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- Authors
- Burton, G. J., Jauniaux, E., & Charnock-Jones, D. S.
- Affiliations
- University of Cambridge (GB)
- Venue
- The International Journal of Developmental Biology
- Publisher
- EHU Press
- Published
- 2010
- Volume
- 54
- Issue
- 2-3
- Pages
- 303-312
- ISSN
- 0214-6282 (ISSN-L)
- OpenAlex
- W2051777630
- Cited by
- 307
- References
- 70
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 12 · 2023: 13 · 2022: 16 · 2021: 27 · 2020: 18 · 2019: 16 · 2018: 17 · 2017: 26 · 2016: 20 · 2015: 20 · 2014: 26 · 2013: 14 · 2012: 28
- FWCI
- 21.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The International Journal of Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wellcome Trust
- Medical Research Council
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Keywords
- placental development, intrauterine environment, first trimester, endometrial glands, nutrient deprivation, trophoblast invasion, vascular compromise, oxidative stress, endoplasmic reticulum stress, unfolded protein response, protein synthesis, mTOR signaling, translation initiation, fetal growth restriction
- MeSH terms
- Female, Humans, Placenta, Placentation, Pregnancy, Protein Biosynthesis, Uterus, Signal Transduction
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