Remarkable placenta

Benirschke, Kurt

doi:10.1002/(sici)1098-2353(1998)11:3<194::aid-ca8>3.0.co;2-t

Cited by 44 publications

(22 citation statements)

References 35 publications

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“…While placental cells (trophoblasts) initially proliferate much more rapidly than the embryo following implantation (6), formation of the maternal-fetal interface and subsequent oxygen and nutrient transport result in a 40-fold increase in the fetus/placenta weight ratio in humans at term (7). This feat is accomplished by a massive increase in placental transport capacity due to a diverse set of developmental processes, including branching and nonbranching angiogenesis, branching morphogenesis, and trophoblast differentiation into several cell types, including invasive cytotrophoblasts (iCTBs) and multinucleated syncytiotrophoblasts (SynTs).…”

mentioning

confidence: 64%

The placenta: transcriptional, epigenetic, and physiological integration during development

Maltepe¹,

Bakardjiev²,

Fisher³

2010

J. Clin. Invest.

248

204

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The placenta provides critical transport functions between the maternal and fetal circulations during intrauterine development. Formation of this interface relies on coordinated interactions among transcriptional, epigenetic, and environmental factors. Here we describe these mechanisms in the context of the differentiation of placental cells (trophoblasts) and synthesize current knowledge about how they interact to generate a functional placenta. Developing an understanding of these pathways contributes to an improvement of our models for studying trophoblast biology and sheds light on the etiology of pregnancy complications and the in utero programming of adult diseases.

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mentioning

confidence: 64%

The placenta: transcriptional, epigenetic, and physiological integration during development

Maltepe¹,

Bakardjiev²,

Fisher³

2010

J. Clin. Invest.

248

204

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“…This hypothesis is also supported by indirect evidence. It has been shown that there is a reduction in the fetus/placenta weight ratio (a marker of placental efficiency) with increased maternal BMI, which is in stark contrast to the 40-fold increase in this value seen from 6 wk of gestation to term in normal pregnancy (9,187). Indeed, reductions in placental efficiency are linked to compensatory increases in placental growth and hypertrophy (7,112).…”

Section: Effects Of Obesity On the Placental Function And Perfusionmentioning

confidence: 99%

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Spradley

Palei

Granger

2015

American Journal of Physiology-Regulatory, Integrative and Comp

112

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) is a pregnancy-specific disorder typically presenting as new-onset hypertension and proteinuria. While numerous epidemiological studies have demonstrated that obesity increases the risk of PE, the mechanisms have yet to be fully elucidated. Growing evidence from animal and human studies implicate placental ischemia in the etiology of this maternal syndrome. It is thought that placental ischemia is brought about by dysfunctional cytotrophoblast migration and invasion into the uterus and subsequent lack of spiral arteriole widening and placental perfusion. Placental ischemia/ hypoxia stimulates the release of soluble placental factors into the maternal circulation where they cause endothelial dysfunction, particularly in the kidney, to elicit the clinical manifestations of PE. The most recognized of these factors are the anti-angiogenic sFlt-1 and pro-inflammatory TNF-␣ and AT1-AA, which promote endothelial dysfunction by reducing levels of the provasodilator nitric oxide and stimulating production of the potent vasoconstrictor endothelin-1 and reactive oxygen species. We hypothesize that obesity-related metabolic factors increase the risk for developing PE by impacting various stages in the pathogenesis of PE, namely, 1) cytotrophoblast migration and placental ischemia; 2) release of soluble placental factors into the maternal circulation; and 3) maternal endothelial and vascular dysfunction. This review will summarize the current experimental evidence supporting the concept that obesity and metabolic factors like lipids, insulin, glucose, and leptin affect placental function and increase the risk for developing hypertension in pregnancy by reducing placental perfusion; enhancing placental release of soluble factors; and by increasing the sensitivity of the maternal vasculature to placental ischemia-induced soluble factors. body mass index; inflammation; placental ischemia; pregnancy; RUPP; sFlt-1 PE IS A PREGNANCY-SPECIFIC DISORDER typically identified by new-onset hypertension in the second half of pregnancy. Although often accompanied by new-onset proteinuria, PE can be associated with many other signs and symptoms including headaches, visual disturbances, epigastric pain, and the development of edema (4,192). Globally, this disease affects over 8 million pregnancies per year and is estimated to account for 40 -60% of maternal deaths in developing countries (125). In the United States, there was a 25% increase in the rate of PE between the years 1987-2004 (189). This significant increase highlights the importance of understanding how risk factors like obesity play a role in the pathogenesis of this maternal syndrome. Obesity is defined as a body mass index (BMI) of greater than or equal to 30 kg/m 2 . Greater than one-half of pregnant women are overweight or obese (48), and more than two-thirds of reproductive-aged women in the United States are overweight or obese (49). Although mounting epidemiological evidence supports obesity as a major risk factor for PE, the mechanisms linking these two morbidities are...

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“…Tantalizingly, this information may even reside within the chorion, as T is also expressed there (Inman and Downs, 2006a). Based on morphology of the mature placenta, the umbilical vasculature is invariably secured onto the central chorionic plate (Benirschke, 1998), which may be in direct register with the embryonic A-P axis. Clinically, central insertion seems important, as umbilical insertions at eccentric sites on the disk are associated with low birthweight, birth defects and fetal morbidity (Benirschke and Kaufmann, 2000).…”

Section: Vascularization Of the Allantois (Lb-onwards; ∼ ‡75 Dpc)mentioning

confidence: 99%

The murine allantois: emerging paradigms in development of the mammalian umbilical cord and its relation to the fetus

Inman

Downs

2007

Genesis

102

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Summary: The fertilized egg of the mammal gives rise to the embryo and its extraembryonic structures, all of which develop in intimate relation with each other. Yet, whilst the past several decades have witnessed a vast number of studies on the embryonic component of the conceptus, study of the extraembryonic tissues and their relation to the fetus have been largely ignored. The allantois, precursor tissue of the mature umbilical cord, is a universal feature of all placental mammals that establishes the vital vascular bridge between the fetus and its mother. The allantois differentiates into the umbilical blood vessels, which become secured onto the chorionic component of the placenta at one end and onto the fetus at the other. In this way, fetal blood is channeled through the umbilical cord for exchange with the mother. Despite the importance of this vascular bridge, little is known about how it is made. The aim of this review is to address current understanding of the biology of the allantois in the mouse and genetic control of its features and functions, and to highlight new paradigms concerning the developmental relationship between the fetus and its umbilical cord. genesis 45: 237-258,

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Remarkable placenta

Cited by 44 publications

References 35 publications

The placenta: transcriptional, epigenetic, and physiological integration during development

The placenta: transcriptional, epigenetic, and physiological integration during development

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

The murine allantois: emerging paradigms in development of the mammalian umbilical cord and its relation to the fetus

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