Colocalisation of Vascular Endothelial Growth Factor and Its Flt-1 Receptor in Human Placenta

Ahmed, Asif; Li, Xiao F.; Dunk, Caroline; Whittle, Martin; Rushton, D. I.; Rollason, T. P.

doi:10.3109/08977199509036883

Cited by 237 publications

(119 citation statements)

References 20 publications

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“…In brief, after incubation with rabbit anti-human NF-B, an HRP-conjugated goat-anti-rabbit Capillaries that were stained along the circumference were recorded as positive. VEGF, VEGF-R1, VEGF-R2, TIE-2, and HIF-1␣ were expressed on all endothelial cells (22,(37)(38)(39). Therefore, the intensity of staining was measured with a three-step semiquantitative scale (magnification ϫ200) as weak (ϩ1), moderate (ϩ2), or strong (ϩ3) (40)…”

Section: Methodsmentioning

confidence: 99%

Decreased Expression of Angiogenic Factors in Placentas with Chorioamnionitis after Preterm Birth

et al. 2005

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Chorioamnionitis and funisitis are associated with neonatal morbidity and mortality. We hypothesized that chorioamnionitis may stress fetal endothelium, activate proinflammatory gene transcription. and affect angiogenic homeostasis in fetal capillaries. Placentas from preterm infants were stained for heat-shock protein 70, nuclear factor-B, hypoxia-inducible factor-1␣, and vascular endothelial growth factor (VEGF). VEGF receptors (VEGF-R) 1 and 2 as well as the receptor tyrosine kinase with immunoglobulin and epidermal growth factor homology domains (TIE-2), which is involved in vascular remodeling, were quantified. Immunohistochemistry was analyzed by counting positive capillaries in placental terminal villi. Staining intensity was quantified by a three-step semiquantitative scale. The samples were divided into three matched groups according to histology: chorioamnionitis with funisitis ("funisitis"), chorioamnionitis without funisitis ("chorioamnionitis"), and control group with no inflammation. In tissues from the funisitis or chorioamnionitis group, heat-shock protein 70 expression was increased over the control group. More nuclear factor-B-positive nuclei of endothelial cells in capillaries were counted in the funisitis and chorioamnionitis groups. Expression of VEGF and VEGF-R1 and -R2 were reduced in cases of funisitis or chorioamnionitis in comparison with controls. Hypoxia-inducible factor-1␣ expression tended to be slightly lower in the funisitis and chorioamnionitis groups but did not reach statistical significance. We speculate that cellular stress and changes in angiogenic homeostasis induced by proinflammatory activation of fetal endothelium in chorioamnionitis may not be limited to the placenta but may also involve other fetal organs. (Pediatr Res 58: 607-612, 2005) Abbreviations BPD, bronchopulmonary dysplasia CI, confidence interval HIF-1␣ hypoxia-inducible factor-1␣ HRP, horseradish peroxidase HSP70, heat-shock protein 70 IL, interleukin NF-B, nuclear factor-B TIE-2, tyrosine kinase with immunoglobulin and epidermal growth factor homology domains-2 VEGF, vascular endothelial growth factor VEGF-R, vascular endothelial growth factor receptor Chorioamnionitis is very common in preterm birth (1). Microbial infection of the amnion and chorion are detected in 60% of all preterm deliveries (2). Funisitis is diagnosed as an infiltration of neutrophils in the umbilical cord vessels (3) and can be considered as a progression of chorioamnionitis with systemic inflammatory response syndrome of the fetus (4). Although fetal inflammation reduces the incidence of respiratory distress syndrome (5,6) and increases the survival of preterm infants (7), the fetal inflammatory response has been associated with increased neonatal morbidity. The mechanisms by which fetal inflammation increases the incidence of bronchopulmonary dysplasia (BPD) (8), retinopathy of prematurity (9), intracranial hemorrhage (10), cerebral palsy, and adverse neurodevelopmental outcome (11-13) are not fully understood. Recently, a new poten...

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Section: Methodsmentioning

confidence: 99%

Decreased Expression of Angiogenic Factors in Placentas with Chorioamnionitis after Preterm Birth

et al. 2005

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“…Previous studies have reported increased VEGFR-1 levels in cases with preeclampsia (1,13,(35)(36)(37)(38). It has also been suggested that high levels of sVEGFR-1 inhibits angiogenesis by antagonising the effects of VEGF and PlGF (39,40). It has also been shown that sVEGFR-1 levels positively correlate with the severity of preeclampsia (1,9).…”

Section: Discussionmentioning

confidence: 83%

The effect of Silymarin on VEGF, VEGFR-1 and IL-1α levels in placental cultures of severe preeclamptic women

Kaya

Başer

Kaya

et al. 2014

J Turkish German Gynecol Assoc

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Objective:The purpose of this study was to evaluate the effects of Silymarin on vascular endothelial growth factor (VEGF), soluble VEGF Receptor-1 (sVEGFR-1) and Interleukin-1 alpha (IL-1α) levels in placental tissue samples of severely preeclamptic women. Material and Methods:We conducted an in vitro study in Başkent University Faculty of Medicine, Ankara, Turkey between September 2008 and May 2009. A total of 16 placental tissue samples (8 from severe preeclamptic, and 8 from controls) were analysed. Placental samples were incubated, and VEGF, sVEGFR-1, and IL1-α were measured in culture media using an ELISA kit. The effect of Silymarin on these levels was investigated. Descriptive statistics were initially performed, followed by Mann Whitney U-test and Kruskal-Wallis test to compare means between groups. P values less than 0.05 were considered statistically significant. Results:Eight patients were included in the severe preeclampsia (SP) group, whereas the remaining 8 patients were included in the control group. There were no significant correlations between gestational age and placental VEGF, sVEGFR-1 and IL-1α after 48 or 72 hours of incubation. Basal VEGF levels were lower in the SP group; however, it did not reach statistical significance. sVEGFR-1 and IL-1α levels were also similar between the SP and control groups (p>0.05). After 48 and 72 hours of incubation, sVEGFR-1 levels in Silymarin-added SP and control placental cultures were lower than in the samples without Silymarin addition; however, this difference also did not reach significance. Conclusion:Although we could not demonstrate a significant effect on placental cytokines, considering the role of vasospasm, inflammation, angiogenesis, endothelial cell activation, and oxidative stress in preeclampsia, the potential benefits of Silymarin should be evaluated in future trials with a larger sample size. (J Turk Ger Gynecol Assoc 2014; 15: 30-5) Key words: Severe preeclampsia, placenta, vascular endothelial growth factor, Silymarin Received: 17 August, 2013 Accepted: 30 September, 2013 The effect of Silymarin on VEGF, VEGFR-1 and IL-1α levels in placental cultures of severe preeclamptic women After obtaining informed consent, severe preeclamptic women who underwent caesarean section above 30 weeks of gestation were prospectively included in the study. Severe preeclampsia (SP) was defined as new-onset hypertension and proteinuria in a >20 week pregnant woman with one or more of the following features: 1) severely elevated blood pressure (systolic ≥160 mmHg and/or diastolic ≥110 mmHg) measured at least twice with a 6 hour interval; 2) proteinuria ≥5 gr in 24-hour collected urine or ≥2+ in dipstick test; 3) serum creatinine ≥1.2 mg/dL; 4) oliguria (<400 cc in 24 hours); 5) thrombocytopenia (<100,000/mm 3 ); 6) microangiopathic haemolysis (Lactate dehydrogenase (LDH) ≥600 U/L or uncongugated bilirubin ≥1.2 mg/dL); 7) impaired liver function tests (Aspartate serum transaminase ≥ twice normal); 8) foetal growth restriction (FGR); 9) symptoms of cent...

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“…Those macrophages will express angiogenic growth factors and, as they appear early, they suggest a paracrine role in the initiation of vasculogenesis. Angiogenic growth factors are also expressed by the maternal decidua and macrophages mediating the trohpoblast invasion [Ahmed et al, 1995]. In the meanwhile since the uterus and its contents demand an increased supply of blood during pregnancy, its vasculature undergoes three main adaptative changes: vasodilation, increased permeability, and growth and development of new vessels.…”

Section: Vessel Growth and Angiogenesismentioning

confidence: 99%

Placental Angiogenesis and Fetal Growth Restriction

Gourvas¹,

Dalpa²,

Vrachnis³

et al. 2012

From Preconception to Postpartum

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Colocalisation of Vascular Endothelial Growth Factor and Its Flt-1 Receptor in Human Placenta

Cited by 237 publications

References 20 publications

Decreased Expression of Angiogenic Factors in Placentas with Chorioamnionitis after Preterm Birth

Decreased Expression of Angiogenic Factors in Placentas with Chorioamnionitis after Preterm Birth

The effect of Silymarin on VEGF, VEGFR-1 and IL-1α levels in placental cultures of severe preeclamptic women

Placental Angiogenesis and Fetal Growth Restriction

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