Endothelial cell expression of adhesion molecules is induced by fetal plasma from pregnancies with umbilical placental vascular disease

Wang, X

doi:10.1016/s1470-0328(02)01240-5

“…Synthesis of proinflammatory cytokines IL‐6 and IL‐8 also occurred 13 . As further evidence these processes were occurring, we showed that fetal plasma from patients with an abnormal umbilical artery Doppler study contained increased levels of IL‐6 and IL‐8 14 and the soluble fractions of the adhesion molecules ICAM‐1 and PECAM‐1 11 . All of these findings pointed to injury of the vascular endothelium in the fetal umbilical placental circulation in cases with high resistance umbilical artery Doppler waveforms.…”

Section: Introductionmentioning

confidence: 52%

“…There were no significant interactions between smoking, route of delivery and gestational age within the study groups for both iNOS and ecNOS expression. In this study, 65 patients were also included in our study of the endothelial cell adhesion molecule expression 11 . Two‐way analysis of variance showed no difference in the three study groups for the common and uncommon patients.…”

Section: Resultsmentioning

confidence: 99%

“…We postulated that these changes in the fetal platelet population would follow contact with activated endothelial cells. Incubation of a standard human umbilical vein endothelial cells (HUVEC) culture with 10% fetal plasma caused endothelial cell expression of adhesion molecules of the immunoglobulin gene superfamily indicative of endothelial cell activation 11 . Apoptosis was increased 12 .…”

Section: Introductionmentioning

confidence: 99%

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Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Wang

¹

,

Wang

²

,

Trudinger³

2003

BJOG

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Objective To determine whether endothelial cell injury would be produced by factor(s) released into the fetal circulation, manifested by altered messenger RNA expression of nitric oxide synthase. Design Case -control study.Setting University teaching hospital.Samples Fetal plasma was collected from 34 normal pregnancies, 44 pregnancies with umbilical placental vascular disease identified by an abnormal umbilical Doppler and 11 pregnancies with maternal pre-eclampsia but with normal umbilical Doppler studies. Methods Aliquots from a common culture of human umbilical vein endothelial cells (HUVECs) were incubated with fetal plasma from the members of the three patient groups. The total RNA was extracted from the endothelial cells and mRNA for nitric oxide synthase was measured by reverse transcription and semi-quantitative polymerase chain reaction (RT-PCR). This was standardised by comparison of the amplified inducible nitric oxide synthase (iNOS) or endothelial constitutive nitric oxide synthase (ecNOS) to glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Main outcome measure Endothelial cell gene expression of iNOS and ecNOS.Results The mRNA expression of iNOS and ecNOS were significantly higher ( P < 0.05) in HUVECs stimulated by fetal plasma from pregnancies with umbilical placental vascular disease [iNOS 1.12 (0.16); ecNOS 1.78 (0.18)] when compared with normal pregnancies [iNOS 0.56 (0.06); ecNOS 1.06 (0.10)]. In the maternal pre-eclampsia group, the NOS expression [iNOS 0.76 (0.11); ecNOS 1.39 (0.26)] did not differ from normal pregnancy. In the vascular disease group, there was no difference in NOS expression between the subgroups with and without maternal pre-eclampsia. Conclusions Our study demonstrates that umbilical placental vascular disease is associated with a factor(s) in fetal plasma that produces an increase in the expression of iNOS and ecNOS mRNA by endothelial cells. Our findings raise the possibility that the release of factors causing an up-regulation of iNOS and ecNOS in the endothelium in the fetal placenta may occur as part of an inflammatory response of the vascular endothelium to injury.

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“…Synthesis of proinflammatory cytokines IL-6 and IL-8 also occurred 13 . As further evidence these processes were occurring, we showed that fetal plasma from patients with an abnormal umbilical artery Doppler study contained increased levels of IL-6 and IL-8 14 and the soluble fractions of the adhesion molecules ICAM-1 and PECAM-1 11 . All of these findings pointed to injury of the vascular endothelium in the fetal umbilical placental circulation in cases with high resistance umbilical artery Doppler waveforms.…”

Section: Introductionmentioning

confidence: 73%

Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Wang¹

2003

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective To determine whether endothelial cell injury would be produced by factor(s) released into the fetal circulation, manifested by altered messenger RNA expression of nitric oxide synthase. Design Case -control study.Setting University teaching hospital.Samples Fetal plasma was collected from 34 normal pregnancies, 44 pregnancies with umbilical placental vascular disease identified by an abnormal umbilical Doppler and 11 pregnancies with maternal pre-eclampsia but with normal umbilical Doppler studies. Methods Aliquots from a common culture of human umbilical vein endothelial cells (HUVECs) were incubated with fetal plasma from the members of the three patient groups. The total RNA was extracted from the endothelial cells and mRNA for nitric oxide synthase was measured by reverse transcription and semi-quantitative polymerase chain reaction (RT-PCR). This was standardised by comparison of the amplified inducible nitric oxide synthase (iNOS) or endothelial constitutive nitric oxide synthase (ecNOS) to glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Main outcome measure Endothelial cell gene expression of iNOS and ecNOS.Results The mRNA expression of iNOS and ecNOS were significantly higher ( P < 0.05) in HUVECs stimulated by fetal plasma from pregnancies with umbilical placental vascular disease [iNOS 1.12 (0.16); ecNOS 1.78 (0.18)] when compared with normal pregnancies [iNOS 0.56 (0.06); ecNOS 1.06 (0.10)]. In the maternal pre-eclampsia group, the NOS expression [iNOS 0.76 (0.11); ecNOS 1.39 (0.26)] did not differ from normal pregnancy. In the vascular disease group, there was no difference in NOS expression between the subgroups with and without maternal pre-eclampsia. Conclusions Our study demonstrates that umbilical placental vascular disease is associated with a factor(s) in fetal plasma that produces an increase in the expression of iNOS and ecNOS mRNA by endothelial cells. Our findings raise the possibility that the release of factors causing an up-regulation of iNOS and ecNOS in the endothelium in the fetal placenta may occur as part of an inflammatory response of the vascular endothelium to injury.

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“…We also showed a factor in fetal plasma from these pregnancies, capable of inducing this change in endothelial cells in culture. 9,10 In this study, we sought to explore further the origin of the vascular pathology identified by the high-resistance umbilical artery Doppler flow velocity waveform. We hypothesised that injury to the endothelium in placental vascular disease would be evidenced by upregulation of the Egr-1 transcription factor.…”

Section: Introductionmentioning

confidence: 99%

Egr‐1 transcription activation exists in placental endothelium when vascular disease is present

Wang

¹

,

Athayde

²

,

Trudinger

³

2006

BJOG

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Objective To seek evidence of early vascular injury in the placental villous microcirculation in placental insufficiency identified by a high-resistance umbilical Doppler study by examining for expression of fibroblast growth factor receptor-1 (FGFR-1), its transcription factor, early growth response factor-1 (Egr-1) and plasma fibroblast growth factor-2 (FGF-2).Design Case-control study.Setting University teaching hospital.Sample Placentas and umbilical vein blood were collected at delivery from 12 women with normal pregnancy delivered at term and 14 with placental vascular disease defined by an abnormal umbilical artery Doppler study.Methods Microvascular endothelial cells were isolated from fresh human placentas using collagenase digestion and Dynabeads coated with monoclonal antibody against CD31. RNA was extracted from the isolated endothelial cells. The messenger RNA (mRNA) expression of FGFR-1 and Egr-1 production were assessed by reverse transcription polymerase chain reaction and factored relative to 18S ribosomal RNA. To confirm that FGF-2 was playing a significant role in this microvascular endothelial cell injury in the placenta, we also measured the soluble fraction of FGF-2 in fetal plasma from same groups of pregnancies using an enzyme-linked immunosorbent assay.

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Endothelial cell expression of adhesion molecules is induced by fetal plasma from pregnancies with umbilical placental vascular disease

Cited by 5 publications

References 24 publications

Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Gene expression of nitric oxide synthase by human umbilical vein endothelial cells: the effect of fetal plasma from pregnancy with umbilical placental vascular disease

Egr‐1 transcription activation exists in placental endothelium when vascular disease is present

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