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Tumor necrosis factor-α regulates angiogenesis of BeWo cells via synergy of PlGF/VEGFR1 and VEGF-A/VEGFR2 axes.

Tumor necrosis factor-alpha (TNF- α) promotes tumor growth by enhancing tumor angiogenesis; however, the effects on choriocarcinoma remain unknown. We investigated the effects of TNF-α on the production of placental growth factor (PlGF) and vascular endothelial growth factor-A (VEGF-A) in BeWo cells and also examined its significance on the interactions with the endothelial cells by using human umbilical vein endothelial cells (HUVECs).

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Serum soluble LIGHT in the early third trimester as a novel biomarker for predicting late-onset preeclampsia.

Our aim was to evaluate whether serum levels of soluble LIGHT (sLIGHT) at 27-31 weeks can predict the later occurrence of gestational hypertension (GH), late-onset preeclampsia (PE), and early-onset PE. Mean blood pressure (MBP), soluble fma-like tyrosine kinase 1/placental growth factor (sFlt-1/PlGF) ratio at 27-31 weeks, and sLIGHT at 27-31 weeks were independent risk factors for late-onset PE. The combination of the three risk factors improved sensitivity with a false-positive rate of 10% (MBP: 60%, log(sFlt-1/PlGF): 45%, sLIGHT: 35%, combination: 75%). Serum sLIGHT in the early third trimester may be a novel biomarker for predicting late-onset PE.

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Activator protein-1 contributes to the NaCl-induced expression of VEGF and PlGF in RPE cells.

Systemic hypertension is a risk factor of neovascular age-related macular degeneration; consumption of dietary salt resulting in extracellular hyperosmolarity is a main cause of hypertension. Extracellular hyperosmolarity was shown to induce expression of angiogenic growth factors, such as vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), in RPE cells. The aim of the present study was to determine whether the hyperosmotic expression of growth factor genes in RPE cells is mediated by activator protein-1 (AP-1), and whether c-Fos and c-Jun genes are regulated by extracellular osmolarity.

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Activation of brown adipocytes by placental growth factor.

Gestational diabetes mellitus (GDM) is a type of diabetes and occurs during pregnancy. Brown adipose tissue (BAT) improves glucose homeostasis and mitigates insulin resistance, however, its activity is reduced in GDM. Placenta growth factor (PlGF) is an angiogenic factor produced by placental trophoblasts. Nevertheless, whether and how PlGF could affect BAT function in GDM are not defined. To investigate this question, 91 non-diabetic pregnant participants and 73 GDM patients were recruited to Gynaecology and Obstetrics Centre in Lu He hospital. Serum levels of PlGF were quantified by ELISA. Skin temperature was measured by far infrared thermography in the supraclavicular region where classical BATs were located. The direct effect of PlGF on BAT function was explored using the established human preadipocyte differentiation system. Thereby, we demonstrated that serum levels of PlGF were lower in GDM patients compared with controls, which was accompanied by decreased skin temperature in the supraclavicular region. By qPCR and western blot, mRNA and protein expression of UCP1 and OXPHOS were elevated in differentiated adipocytes treated with PlGF. PlGF stimulated mitochondrion transcription and increased copy number of mitochondrial. When subjected for respirometry, PlGF-treated differentiated adipocytes showed higher oxygen consumption rates than controls. PlGF induced AMPK phosphorylation and blockade of AMPK phosphorylation blunted UCP1 and OXPHOS expression in differentiated adipocytes. PlGF administration reduced cholesterol and triglyceride content in the liver and improved insulin sensitivity in db mice compared with control. In Conclusion, PlGF could activate BAT function. Downregulation of PlGF might contribute to the reduced BAT activity in GDM.

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Modulation of trophoblast function by concurrent hyperglycemia and antiphospholipid antibodies is in part TLR4-dependent.

While diabetes and APS are individually associated with increased risk of poor perinatal outcomes, in particular preeclampsia, recent studies have demonstrated an association between concurrent aPL and diabetes leading to an increased risk of pregnancy morbidity. Hyperglycemia and aPL have independently been shown to alter human trophoblast function by inducing a pro-inflammatory, anti-angiogenic, and antimigratory response. However, little is known about the effects of concurrent hyperglycemia and aPL on trophoblast function.

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The expression of serum sEGFR, sFlt-1, sEndoglin and PLGF in preeclampsia.

The objective of this study was to investigate soluble epidermal growth factor receptor (sEGFR), soluble vascular endothelial growth factor receptor 1 (sFlt-1), soluble endoglin (sEndoglin) and placenta growth factor (PLGF) concentrations in normotensive, preterm and term preeclamptic pregnancies' serum and thus to specify the clinical utility of these biochemical markers in monitoring severity and intrauterine growth retardation of preterm preeclampsia. 172 pregnant women were divided into the following groups: preterm preeclampsia, preterm control, term preeclampsia and term control. Preterm preeclampsia patients were stratified with severe feature (n = 50) and without severe feature (n = 22). sEGFR, sEndoglin and PLGF were assessed using Luminex multiplex immunoassay, whilesFlt-1 was assessed using ELISA. sEGFR was significantly lower in preterm preeclampsia than matched control (p < 0.001) and mildly lower in term preeclampsia than matched control (p < 0.01). On contrary, sFlt-1 was significantly higher in preterm preeclampsia than matched control (p < 0.001) and mildly higher in term preeclampsia than matched control (p < 0.01). sFlt-1, sFlt-1/sEGFR and sFlt-1/PLGF were positively correlated with the severity of preterm preeclampsia (P < 0.001, R value ≥ 0.6), especially sFlt-1/sEGFR had the highest R value (R value = 0.711) among them. Furthermore, sEndoglin and the ratio of sEndoglin/sEGFR were associated with neonatal birth weight small for gestational age (SGA, n = 25) in preterm preeclampsia group.

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Effect of sildenafil citrate on circulating levels of sFlt-1 in preeclampsia.

To examine the effect of sildenafil on level of antiangiogenic proteins of preeclampsia. Firstly to examine the effect of sildenafil on serum biomarkers in a patient with preterm preeclampsia. Secondly, to examine the effect of sildenafil on sFlt-1 and soluble endoglin secretion from primary trophoblasts and placental explants.

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Excess glucose induce trophoblast inflammation and limit cell migration through HMGB1 activation of Toll-Like receptor 4.

Hyperglycemia increases the risk of preeclampsia. Hyperglycemia induces a placental trophoblast inflammatory (IL-1β, IL-6, IL-8), antiangiogenic (sFlt-1, sEndoglin), and anti-migratory profile. The IL-1β response is mediated via inflammasome activation by the damage-associated molecular pattern (DAMP), uric acid. The objective of this study was to determine the role of high-mobility group box-1 (HMGB1), a DAMP that activates Toll-like receptor 4 (TLR4), in human first trimester trophoblast responses to hyperglycemia. The trophoblast response to excess glucose under different oxygen tensions was also investigated.

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Upregulation of Angiogenic Factors via Protein Kinase C and Hypoxia-induced Factor-1α Pathways under High-glucose Conditions in the Placenta.

Abnormal glucose metabolism during pregnancy is an established risk factor for preeclampsia (PE). Disruption of the balance between placental angiogenic factors is linked to PE pathophysiology. We examined whether hypoxia-induced factor-1α (HIF-1α) and protein kinase Cβ (PKCβ) are involved in the regulation of placental angiogenic factors under high-glucose conditions in vitro. The human choriocarcinoma cell lines BeWo and JEG-3, and the human trophoblast cell line HTR-8/SVneo were cultured with 10 and 25 mmol/L glucose [control glucose group (CG) and high-glucose group (HG), respectively]. We examined the changes in HIF-1α, soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), and vascular endothelial growth factor (VEGF) expression in the CG and HG by real-time PCR and ELISA. PKC activation was also measured by ELISA. The expressions of HIF-1α, sFlt-1, PlGF, and VEGF were significantly higher in the HG than in the CG. PKC activity was significantly increased in the HG. High glucose affected the expression of angiogenic factors in choriocarcinoma cells via the PKCβ and HIF-1α pathways, suggesting their involvement in PE pathogenesis.

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Angiogenic profile in the Finnish Genetics of Pre-Eclampsia Consortium (FINNPEC) cohort.

To study first and second/third trimester levels of soluble fms-like tyrosine kinase 1 (sFlt1), placental growth factor (PlGF) and soluble endoglin (sEng) in FINNPEC case-control cohort. The participants were further divided into subgroups based on parity and onset of the disease. Recommended cut-off values in aid of pre-eclampsia (PE) prediction and diagnosis were also tested.

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