Human embryo modulates placental function in the first trimester; Effects of neural tissues upon chorionic gonadotropin and progesterone secretion

Shurtz-Swirski, Revital; Simon, Robert R.; Cohen, Yael Helfman; Barnea, Eytan R.

doi:10.1016/0143-4004(91)90028-e

Cited by 9 publications

(3 citation statements)

References 16 publications

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“…Although is has been shown that women with naturally higher levels of antioxidant enzymes are less likely to miscarry (Baxter et al, 2001), the impact of peri-conceptional antioxidant supplementation on early pregnancy failure rates in the general population remains to be investigated. Theoretically, major fetal abnormalities leading to fetal demise within the first 2 months of pregnancy could also lead to a secondary placental dysfunction as the placental development becomes increasingly dependent on fetal synthesis towards the end of the first trimester (Shurtz-Swirski et al, 1991). This may be modulated by tumour necrosis factor (TNF)-α, a multifunctional cytokine which has been identified in the maternal reproductive tract, the placenta and fetal tissues (Toder et al, 2003).…”

Section: Miscarriages and Oxidative Stressmentioning

confidence: 99%

Placental-related diseases of pregnancy: involvement of oxidative stress and implications in human evolution

Jauniaux¹,

Poston²,

Burton³

2006

Human Reproduction Update

524

380

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Miscarriage and pre-eclampsia are the most common disorders of human pregnancy. Both are placental-related and exceptional in other mammalian species. Ultrasound imaging has enabled events during early pregnancy to be visualized in vivo for the first time. As a result, a new understanding of the early materno-fetal relationship has emerged and, with it, new insight into the pathogenesis of these disorders. Unifying the two is the concept of placental oxidative stress, with associated necrosis and apoptosis of the trophoblastic epithelium of the placental villous tree. In normal pregnancies, the earliest stages of development take place in a low oxygen (O2) environment. This physiological hypoxia of the early gestational sac protects the developing fetus against the deleterious and teratogenic effects of O2 free radicals (OFRs). In miscarriage, development of the placento-decidual interface is severely impaired leading to early and widespread onset of maternal blood flow and major oxidative degeneration. This mechanism is common to all miscarriages, with the time at which it occurs in the first trimester depending on the aetiology. In contrast, in pre-eclampsia the trophoblastic invasion is sufficient to allow early pregnancy phases of placentation but too shallow for complete transformation of the arterial utero-placental circulation, predisposing to a repetitive ischaemia-reperfusion (I/R) phenomenon. We suggest that pre-eclampsia is a three-stage disorder with the primary pathology being an excessive or atypical maternal immune response. This would impair the placentation process leading to chronic oxidative stress in the placenta and finally to diffuse maternal endothelial cell dysfunction.

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Section: Miscarriages and Oxidative Stressmentioning

confidence: 99%

Placental-related diseases of pregnancy: involvement of oxidative stress and implications in human evolution

Jauniaux¹,

Poston²,

Burton³

2006

Human Reproduction Update

524

380

View full text Add to dashboard Cite

show abstract

“…Most chromosomal abnormalities are associated with primary abnormal trophoblast invasion of the uterine decidua [5–7]. As the placental development becomes increasingly dependent on fetal synthesis towards the end of the first trimester, isolated major fetal structural defects leading to early fetal demise can also lead to secondary placental dysfunction causing a miscarriage [8]. …”

Section: Introductionmentioning

confidence: 99%

Inflammatory Cytokines in Maternal Circulation and Placenta of Chromosomally Abnormal First Trimester Miscarriages

Calleja‐Agius

Jauniaux

Muttukrishna

2012

Clinical and Developmental Immunology

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The impact of abnormal placental karyotype on the inflammatory response within the villous tissue and peripheral circulation of women with miscarriage was evaluated. Villous (n = 38) and venous blood samples (n = 26) were obtained from women with missed miscarriage. Tissue chromosome analysis indicated 23 abnormal and 15 normal karyotypes. Concentration of tumour necrosis factor alpha (TNFα), TNF-R1 and TNF-R2, and interleukin (IL)-10 were measured using flowcytometric bead array in fresh villous homogenate, cultured villous extracts, culture medium, maternal whole blood, and plasma. Plasma TNFα/IL-10 ratios were significantly (P < 0.05) lower in miscarriages with abnormal karyotype. In the abnormal karyotype group, there were significantly higher levels of TNFα (P < 0.01), IL-10 (P < 0.01), TNF-R1 (P < 0.001), and TNF-R2 (P < 0.001) in the villous extracts and culture-conditioned medium compared to normal karyotype group. In miscarriage with abnormal karyotype, there is an exacerbated placental inflammatory response, in contrast to miscarriage of normal karyotype where maternal systemic response is increased.

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“…Finally, embryo-derived secretory products acting on the uterine milieu may provide protection during gestation and possibly prevent disorders that can manifest long after birth. Evidence for such a protective effect derives from experimental observations that trophoblastic cells, and the embryo, effectively inactivate xenobiotics [4-9]. …”

Section: Introductionmentioning

confidence: 99%

PreImplantation factor (PIF*) promotes embryotrophic and neuroprotective decidual genes: effect negated by epidermal growth factor

Duzyj

Paidas

JeBailey

et al. 2014

J Neurodevelop Disord

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BackgroundIntimate embryo-maternal interaction is paramount for pregnancy success post-implantation. The embryo follows a specific developmental timeline starting with neural system, dependent on endogenous and decidual factors. Beyond altered genetics/epigenetics, post-natal diseases may initiate at prenatal/neonatal, post-natal period, or through a continuum. Preimplantation factor (PIF) secreted by viable embryos promotes implantation and trophoblast invasion. Synthetic PIF reverses neuroinflammation in non-pregnant models. PIF targets embryo proteins that protect against oxidative stress and protein misfolding. We report of PIF’s embryotrophic role and potential to prevent developmental disorders by regulating uterine milieu at implantation and first trimester.MethodsPIF’s effect on human implantation (human endometrial stromal cells (HESC)) and first-trimester decidua cultures (FTDC) was examined, by global gene expression (Affymetrix), disease-biomarkers ranking (GeneGo), neuro-specific genes (Ingenuity) and proteins (mass-spectrometry). PIF co-cultured epidermal growth factor (EGF) in both HESC and FTDC (Affymetrix) was evaluated.ResultsIn HESC, PIF promotes neural differentiation and transmission genes (TLX2, EPHA10) while inhibiting retinoic acid receptor gene, which arrests growth. PIF promotes axon guidance and downregulates EGF-dependent neuroregulin signaling. In FTDC, PIF promotes bone morphogenetic protein pathway (SMAD1, 53-fold) and axonal guidance genes (EPH5) while inhibiting PPP2R2C, negative cell-growth regulator, involved in Alzheimer’s and amyotrophic lateral sclerosis. In HESC, PIF affects angiotensin via beta-arrestin, transforming growth factor-beta (TGF-β), notch, BMP, and wingless-int (WNT) signaling pathways that promote neurogenesis involved in childhood neurodevelopmental diseases—autism and also affected epithelial-mesenchymal transition involved in neuromuscular disorders. In FTDC, PIF upregulates neural development and hormone signaling, while downregulating genes protecting against xenobiotic response leading to connective tissue disorders.In both HESC and FTDC, PIF affects neural development and transmission pathways. In HESC interactome, PIF promotes FUS gene, which controls genome integrity, while in FTDC, PIF upregulates STAT3 critical transcription signal. EGF abolished PIF’s effect on HESC, decreasing metalloproteinase and prolactin receptor genes, thereby interfering with decidualization, while in FTDC, EGF co-cultured with PIF reduced ZHX2, gene that regulates neural AFP secretion.ConclusionsPIF promotes decidual trophic genes and proteins to regulate neural development. By regulating the uterine milieu, PIF may decrease embryo vulnerability to post-natal neurodevelopmental disorders. Examination of PIF-based intervention strategies used during embryogenesis to improve pregnancy prognosis and reduce post-natal vulnerability is clearly in order.

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Human embryo modulates placental function in the first trimester; Effects of neural tissues upon chorionic gonadotropin and progesterone secretion

Cited by 9 publications

References 16 publications

Placental-related diseases of pregnancy: involvement of oxidative stress and implications in human evolution

Placental-related diseases of pregnancy: involvement of oxidative stress and implications in human evolution

Inflammatory Cytokines in Maternal Circulation and Placenta of Chromosomally Abnormal First Trimester Miscarriages

PreImplantation factor (PIF*) promotes embryotrophic and neuroprotective decidual genes: effect negated by epidermal growth factor

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