Understanding placental nutrient transfer – why bother? New biomarkers of fetal growth

Sibley, Colin P.

doi:10.1113/jphysiol.2009.172403

Cited by 83 publications

(53 citation statements)

References 64 publications

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“…19 The capacity of syncytiotrophoblast to perform endothelium-like functions such as controlling substrate exchange across the villous surface has been established. 20,21 Thus, choriocarcinoma assumes the physiology of normal trophoblast and operates its blood supply through tumor syncytiotrophoblast-formed blood vessels. To assess whether syncytiotrophoblast is critically associated with pseudovascularization, we also analyzed other gestational trophoblastic neoplasia including placental site trophoblastic tumor and epithelioid trophoblastic tumor because in these tumors the trophoblastic cells are of intermediate trophoblastic type and, unlike cytotrophoblastic cells, do not generally differentiate into syncytiotrophoblast.…”

Section: Discussionmentioning

confidence: 99%

Trophoblastic vasculogenic mimicry in gestational choriocarcinoma

Shih

2011

Modern Pathology

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Angiogenesis is a characteristic feature of solid tumors, which depend on the newly formed vasculature to prevent hypoxia and to sustain uncontrolled tumor cell proliferation. In this study, we investigated the blood supply system in 10 gestational choriocarcinomas on the basis of histopathological and immunohistochemical features. In all examined cases, morphological analysis demonstrated that blood channels within the center of choriocarcinomas were surrounded by neoplastic trophoblastic cells rather than by endothelial cells. Similarly, there was a lack of CD31 and CD34-positive endothelial cells within choriocarcinomas. In the periphery of choriocarcinomas, tumor cells invaded uterine stroma-derived blood vessels where trophoblastic cells replaced endothelial cells, forming anastomoses between endothelium-lined blood vessels and trophoblastlined pseudovascular channels. Masson's trichrome staining revealed minimal amounts of connective tissue within choriocarcinomas. In contrast, CD31 and CD34-positive blood vessels were present in other types of gestational trophoblastic neoplasms including 8 placental site trophoblastic tumors and 12 epithelioid trophoblastic tumors. These findings provide cogent evidence that choriocarcinoma represents one of a few human tumor types that utilizes vasculogenic mimicry by tumor cell in supporting tumor development.

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Section: Discussionmentioning

confidence: 99%

Trophoblastic vasculogenic mimicry in gestational choriocarcinoma

Shih

2011

Modern Pathology

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“…It also provides hormones and growing factors that modulate fetal and placental growth and development (Jones et al 2007, Sibley 2009). Thus, placental expression and the activity of specific transporters will determine the maternal-fetal transport of nutrients.…”

Section: Introductionmentioning

confidence: 99%

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Mazzucco

Higa

Capobianco

et al. 2013

Journal of Endocrinology

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Metabolic alterations in obese and overweight mothers impact the placenta and the fetus, leading to anomalies in fetal growth and lipid accretion. The primary aim of the study was to examine the effect of a saturated fat-rich diet (FD) on growth, lipid accretion, and lipases, leptin and leptin receptor (ObR) expression in the placenta and fetal liver. We also aimed to find a role for fetal leptin in the modulation of placental and fetal liver lipase and ObR expression. Six-week-old rats were fed with a standard rat chow (control) or a 25% FD for 7 weeks until mating and during pregnancy. Also, in a group of control rats, fetuses were injected with leptin on days 19, 20, and 21 of pregnancy. On day 21, we assessed lipidemia, insulinemia, and leptinemia in mothers and fetuses. In the placenta and fetal liver, lipid concentration was assessed by thin layer chromatography (TLC) and the gene expression of lipoprotein lipase (LPL), endothelial lipase, insulin receptor (Insr), leptin, and ObR by RT-PCR. The FD induced hypertriglyceridemia and hyperleptinemia (P!0.01) in mothers and fetuses, an increase in maternal (P!0.05) and fetal weight (P!0.01), overaccumulation of lipids in fetal liver (P!0.01), and enhanced leptin expression in the placenta and fetal liver (P!0.05). Placental expression of IR and LPL was increased (P!0.05), and ObR decreased (P!0.05) in the FD group. Fetal administration of leptin induced the placental and fetal liver downregulation of ObR (P!0.05) and upregulation of LPL expression (P!0.05). The FD led to increased fetal lipid levels, which may result from high maternal lipid availability and fetal leptin effects. Key Words" Saturated fat-rich diet

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“…Recent data suggest (reviewed in ref. 17) that of these placental changes, some are likely to be causative and others to be adaptive to the growth restriction.…”

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confidence: 99%

“…In human FGR, the activity of a number of different placental solute transporters has now been investigated and compared with that in normal pregnancy (17). Various changes in transporter activities have been observed in FGR: some lowered (e.g., System A, as described above), some not changing (e.g., glucose transporter), and interestingly one transporter, Ca 2+ ATPase, showing increased activity in the basal (fetal facing) plasma membrane of the syncytiotrophoblast.…”

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confidence: 99%

Placental-specific Igf2 knockout mice exhibit hypocalcemia and adaptive changes in placental calcium transport

Dilworth¹,

Kusinski²,

Cowley³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Evidence is emerging that the ability of the placenta to supply nutrients to the developing fetus adapts according to fetal demand. To examine this adaptation further, we tested the hypothesis that placental maternofetal transport of calcium adapts according to fetal calcium requirements. We used a mouse model of fetal growth restriction, the placental-specific Igf2 knockout (P0) mouse, shown previously to transiently adapt placental System-A amino acid transporter activity relative to fetal growth. Fetal and placental weights in P0 mice were reduced when compared with WT at both embryonic day 17 (E17) and E19. Ionized calcium concentration [Ca 2+ ] was significantly lower in P0 fetal blood compared with both WT and maternal blood at E17 and E19, reflecting a reversal of the fetomaternal [Ca 2+ ] gradient. Fetal calcium content was reduced in P0 mice at E17 but not at E19. Unidirectional maternofetal calcium clearance ( Ca K mf ) was not different between WT and P0 at E17 but increased in P0 at E19. Expression of the intracellular calcium-binding protein calbindin-D 9K , previously shown to be rate-limiting for calcium transport, was increased in P0 relative to WT placentas between E17 and E19. These data show an increased placental transport of calcium from E17 to E19 in P0 compared to WT. We suggest that this is an adaptation in response to the reduced fetal calcium accumulation earlier in gestation and speculate that the ability of the placenta to adapt its supply capacity according to fetal demand may stretch across other essential nutrients.fetal growth restriction | calbindin | PMCA | pregnancy

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Understanding placental nutrient transfer – why bother? New biomarkers of fetal growth

Cited by 83 publications

References 64 publications

Trophoblastic vasculogenic mimicry in gestational choriocarcinoma

Trophoblastic vasculogenic mimicry in gestational choriocarcinoma

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Placental-specific Igf2 knockout mice exhibit hypocalcemia and adaptive changes in placental calcium transport

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