Localisation of Placenta Growth Factor (PlGF) in Human Term Placenta

Khaliq, Asud; Li, Xiao F.; Shams, M.; Sisi, Paraskevi; Acevedo, Carmen A.; Whittle, Martin; Weigh, Herbert; Ahmed, Asif

doi:10.3109/08977199609003225

Cited by 179 publications

(99 citation statements)

References 15 publications

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“…The term placenta, which is large in size and thus has a large surface area of trophoblast, contained a consistently strong signal for PlGF mRNA. Khaliq et al (1996) and Vuorela et al (1997) also found PlGF mRNA in the term villus but did not investigate other stages of pregnancy. The abundant PlGF mRNA is likely to lead to significant quantities of PlGF protein being produced, and this is confirmed by the fact that immunoreactive PlGF can readily be detected in maternal circulation during pregnancy (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Comparison of expression patterns for placenta growth factor, vascular endothelial growth factor (VEGF), VEGF-B and VEGF-C in the human placenta throughout gestation

Clark

Smith²,

Licence³

et al. 1998

Journal of Endocrinology

190

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Section: Discussionmentioning

confidence: 99%

Comparison of expression patterns for placenta growth factor, vascular endothelial growth factor (VEGF), VEGF-B and VEGF-C in the human placenta throughout gestation

Clark

Smith²,

Licence³

et al. 1998

Journal of Endocrinology

190

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“…Human PlGF is essentially expressed in the placenta, 26 more precisely in the syncytiotrophoblast. 1 PlGF is a potent stimulator of placental angiogenesis. 3,27 These new data provide 1 mechanism by which biomechanical forces induced by maternal blood flow, that is FSS, could modulate the angiogenic potential of the syncytiotrophoblast.…”

Section: Discussionmentioning

confidence: 99%

“…1 PlGF is a member of the vascular endothelial growth factor (VEGF) family and is crucial in initiating and perpetuating placental angiogenesis. 2 PlGF also induces vasodilation of uterine and myometrial arteries contributing to uterine vascular remodeling 3 and is associated with the systemic maternal cardiovascular adaptations to pregnancy.…”

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confidence: 99%

Fluid Shear Stress Promotes Placental Growth Factor Upregulation in Human Syncytiotrophoblast Through the cAMP–PKA Signaling Pathway

et al. 2016

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Abstract-The effects of fluid shear stress (FSS) on the human syncytiotrophoblast and its biological functions have never been studied. During pregnancy, the syncytiotrophoblast is the main source of placental growth factor (PlGF), a proangiogenic factor involved in the placental angiogenesis and the vascular adaptation to pregnancy. The role of FSS in regulating PlGF expression in syncytiotrophoblasts is unknown. We investigated the impact of FSS on the production and secretion of the PlGF by the human syncytiotrophoblasts in primary cell culture. Laminar and continuous FSS (1 dyn cm −2) was applied to human syncytiotrophoblasts cultured in a parallel-plate flow chambers. Secreted levels of PlGF, sFlt-1 (soluble fmslike tyrosin kinase-1), and prostaglandin E2 were tested by immunologic assay. PlGF levels of mRNA and intracellular protein were examined by RT-PCR and Western blot, respectively. Intracellular cAMP levels were examined by timeresolved fluorescence resonance energy transfer cAMP accumulation assay. Production of cAMP and PlGF secretion was significantly increased in FSS conditions compared with static conditions. Western blot analysis of cell extracts exposed to FSS showed an increased phosphorylation of protein kinase A substrates and cAMP response element-binding protein on serine 133. FSS-induced phosphorylation of cAMP response element-binding protein and upregulation of PlGF were prevented by inhibition of protein kinase A with H89 (3 μmol/L). FSS also triggers intracellular calcium flux, which increases the synthesis and release of prostaglandin E2. The enhanced intracellular cAMP in FSS conditions was blocked by COX1/COX2 (cyclooxygenase) inhibitors, suggesting that the increase in prostaglandin E2 production could activate the cAMP/protein kinase A pathway in an autocrine/paracrine fashion. FSS activates the cAMP/protein kinase A pathway leading to upregulation of PlGF in human syncytiotrophoblast.

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“…Recently, it has been proposed that serial determinations of the concentrations of sVEGFR-1 [38,39], PlGF [38], and s-Eng [39] are more informative in assessing the risk for PE than are single measurements in the first or second trimester. This is plausible because PlGF, s-Eng, and sVEGFR-1 are produced by the trophoblast [23,[39][40][41][42][43][44] and, therefore, maternal plasma concentrations can change with placental development from the first to the second trimester.…”

mentioning

confidence: 99%

The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age

Erez

Romero

Espinoza

et al. 2008

The Journal of Maternal-Fetal & Neonatal Medicine

273

233

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The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age, The Journal of Maternal-Fetal & Neonatal Medicine, 21:5, 279-287, DOI: 10.1080 AbstractIntroduction. An imbalance between angiogenic and anti-angiogenic factors has been proposed as central to the pathophysiology of preeclampsia (PE). Indeed, patients with PE and those delivering small-for-gestational age (SGA) neonates have higher plasma concentrations of soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) and the soluble form of endoglin (s-Eng), as well as lower plasma concentrations of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) than do patients with normal pregnancies. Of note, this imbalance has been observed before the clinical presentation of PE or the delivery of an SGA neonate. The objective of this study was to determine if changes in the profile of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters are associated with a high risk for the subsequent development of PE and/or delivery of an SGA neonate. Methods. This longitudinal case-control study included 402 singleton pregnancies in the following groups: (1) normal pregnancies with appropriate for gestational age (AGA) neonates (n ¼ 201); (2) patients who delivered an SGA neonate (n ¼ 145); and (3) patients who developed PE (n ¼ 56). Maternal plasma samples were obtained at the time of each prenatal visit, scheduled at 4-week intervals from the first or early second trimester until delivery. In this study, we included two samples per patient: (1) first sample obtained between 6 and 15 weeks of gestation ('first trimester' sample), and (2) second sample obtained between 20 and 25 weeks of gestation ('second trimester' sample). Plasma concentrations of s-Eng, sVEGFR-1, and PlGF were determined by specific and sensitive immunoassays. Changes in the maternal plasma concentrations of these angiogenesis-related factors were compared among normal patients and those destined to develop PE or deliver an SGA neonate while adjusting for maternal age, nulliparity, and body mass index. General linear models and polytomous logistic regression models were used to relate the analyte concentrations, ratios, and product to the subsequent development of PE and SGA. Results.(1) An increase in the maternal plasma concentration of s-Eng between the first and second trimesters conferred risk for the development of preterm PE and SGA (OR 14.9, 95% CI 4.9-45.0 and OR 2.9, 95% CI 1.5-5.6, respectively).(2) An increase in the maternal plasma concentration of sVEGFR-1 between the first and second trimester conferred risk for the development of preterm PE (OR 3.9, 95% CI 1.2-12.6). (3) A subnormal increase in maternal plasma PlGF concentration between the first and the second trimester was a risk factor for the subsequent development of preterm and term PE (OR 4....

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Localisation of Placenta Growth Factor (PlGF) in Human Term Placenta

Cited by 179 publications

References 15 publications

Comparison of expression patterns for placenta growth factor, vascular endothelial growth factor (VEGF), VEGF-B and VEGF-C in the human placenta throughout gestation

Comparison of expression patterns for placenta growth factor, vascular endothelial growth factor (VEGF), VEGF-B and VEGF-C in the human placenta throughout gestation

Fluid Shear Stress Promotes Placental Growth Factor Upregulation in Human Syncytiotrophoblast Through the cAMP–PKA Signaling Pathway

The change in concentrations of angiogenic and anti-angiogenic factors in maternal plasma between the first and second trimesters in risk assessment for the subsequent development of preeclampsia and small-for-gestational age

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