Placenta weight in pre‐eclampsia

Dahlstrøm, Berit; Romundstad, Pål Richard; Øian, Pål; Vatten, Lars J.; Eskild, Anne

doi:10.1080/00016340802056178

Cited by 73 publications

(46 citation statements)

References 11 publications

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“…These results might indicate a differential capacity for feto-placental angiogenesis in both pathological conditions. Supporting this idea, it has been described that placental histological changes related to reduced perfusion [10][11][12][13] and reduced placental expression of several pro-angiogenic factors [14,15] are mainly observed in EOPE rather than LOPE. The underlying causes for this behavior are unclear, but considering that adenosine is a well-characterized pro-angiogenic molecule, its level is increased in preeclampsia and the inhibitory ZM-21680-mediated effect on NO and VEGF observed in this study, we propose that adenosine via A 2A AR is conducting the proliferation/migration of HUVEC in LOPE.…”

Section: Discussionmentioning

confidence: 59%

“…Specifically, Doppler studies reveal that impaired feto-placental blood flow is mainly evident in women with early-onset preeclampsia (EOPE) [8] rather than late-onset preeclampsia (LOPE) [9]. Moreover, EOPE exhibits placental histological changes related with reduced perfusion [10][11][12][13] as well as the anomalous structure of the peripheral villi and vasculature compared to respective controls identified by stereological analysis following EOPE, but not LOPE [13]. In addition, low placental levels of several pro-angiogenic factors have been reported in EOPE compared to LOPE or age-matched controls [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

Escudero

Bertoglia

Hernadez

et al. 2012

Purinergic Signalling

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To investigate whether fetal endothelial cell proliferation and migration are modulated by the A 2A adenosine receptor (A 2A AR), nitric oxide (NO) and the vascular endothelial growth factor (VEGF) signaling pathway, we isolated human umbilical vein endothelial cells from normal pregnancy (n023), preterm delivery (n04), and late-onset (LOPE, n010) and early-onset preeclampsia (EOPE, n08). We used the non-selective adenosine receptor agonist (NECA) and the selective agonist (CGS-21680) and/or selective antagonist (ZM-241385) for A 2A AR. Also, the nitric oxide synthase (NOS) inhibitor, L-NAME, was used in co-incubation with CGS-21680. Compared to normal pregnancy, EOPE exhibited low cell proliferation and migration associated with reduced expressions of A 2A AR and VEGF and NO synthesis (i.e., total and phosphorylated serine 1177 endothelial NOS and nitrite formation). In contrast, LOPE exhibited the opposite behavior in all these markers compared to normal pregnancy or EOPE. Cell proliferation and migration were increased by CGS-21680 (or NECA) in all analyzed groups (EOPE>LO-PE>normal pregnancy) compared to their respective basal conditions, an effect that was associated with high NO and VEGF synthesis and blocked by ZM-241385 with significantly different IC 50 for each group (EOPE>LOPE>normal pregnancy). The differences seem independent of gestational age.L-NAME blocked the CGS-21680-mediated cell proliferation and migration in normal pregnancy and LOPE (IC 50 036.2± 2.5 and 8.6±2.2 nM, respectively) as well as the VEGF expression in normal pregnancy. Therefore, the A 2A AR/NO/ VEGF signaling pathway exhibits a pro-angiogenic effect in normal pregnancies and LOPE, whereas impairment in this pathway seems related to the reduced angiogenic capacity of the fetal endothelium in EOPE.

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Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

Escudero

Bertoglia

Hernadez

et al. 2012

Purinergic Signalling

View full text Add to dashboard Cite

show abstract

“…) predicted to compromise intervillous perfusion in advanced/term pregnancy and likely induce a degree of ischemia/reperfusion injury, oxidative stress, inflammation, and acute atherosis similarly to those seen in early-onset PE placentas (Fogarty et al, 2013). This chorionic villous congestion and subsequent syncytial trophoblastic oxidative stress is suggested to underlie late-onset PE, larger placentas (Dahlstrom et al, 2008;Lisonkova and Joseph, 2013) and well-grown, or even large for date, neonates (Xiong et al, 2002;Redman et al, 2014). However, it is worthwhile to remember that early-and late-onset PE should not be considered an 'all-or-none phenomenon' Verlohren et al, 2014).…”

Section: Altered Trophoblast Invasion and Pementioning

confidence: 93%

PreImplantation Factor (PIF*) endogenously prevents preeclampsia: Promotes trophoblast invasion and reduces oxidative stress

Barnea

Vialard

Moindjie

et al. 2016

Journal of Reproductive Immunology

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“…Thus, in addition to low aldosterone levels, compromised deactivation of cortisol exposes the placenta to enhanced cortisol availability further diminishing placental growth. Our data suggest that in preeclampsia, mutually reduced aldosterone and increased cortisol availability might well entail the smaller placental weight associated with the disease (39). Whether this reasoning is entirely correct deserves consideration for the following reason.…”

Section: Figmentioning

confidence: 99%

Regulation of Placental Growth by Aldosterone and Cortisol

et al. 2011

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During pregnancy, trophoblasts grow to adapt the feto-maternal unit to fetal requirements. Aldosterone and cortisol levels increase, the latter being inactivated by a healthy placenta. By contrast, preeclamptic placental growth is reduced while aldosterone levels are low and placental cortisol tissue levels are high due to improper deactivation. Aldosterone acts as a growth factor in many tissues, whereas cortisol inhibits growth. We hypothesized that in preeclampsia low aldosterone and enhanced cortisol availability might mutually affect placental growth and function. Proliferation of cultured human trophoblasts was time-and dose-dependently increased with aldosterone (P Ͻ 0.04 to P Ͻ 0.0001) and inhibited by spironolactone and glucocorticoids (P Ͻ 0.01). Mineralo-and glucocorticoid receptor expression and activation upon agonist stimulation was verified by visualization of nuclear translocation of the receptors. Functional aldosterone deficiency simulated in pregnant mice by spironolactone treatment (15 g/g body weight/day) led to a reduced fetal umbilical blood flow (P Ͻ 0.05). In rat (P Ͻ 0.05; R 2 ϭ 0.2055) and human (X 2 ϭ 3.85; P ϭ 0.0249) pregnancy, placental size was positively related to plasma aldosterone. Autocrine production of these steroid hormones was excluded functionally and via the absence of specific enzymatic transcripts for CYP11B2 and CYP11B1. In conclusion, activation of mineralocorticoid receptors by maternal aldosterone appears to be required for trophoblast growth and a normal feto-placental function. Thus, low aldosterone levels and enhanced cortisol availability may be one explanation for the reduced placental size in preeclampsia and related disorders. (Endocrinology 152: 263-271, 2011)

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Placenta weight in pre‐eclampsia

Cited by 73 publications

References 11 publications

Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

PreImplantation Factor (PIF*) endogenously prevents preeclampsia: Promotes trophoblast invasion and reduces oxidative stress

Regulation of Placental Growth by Aldosterone and Cortisol

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