Maternal Vascular Lesions in Pre-eclampsia and Intrauterine Growth Retardation

Hustin, J.; Foidart, J.M.; Lambotte, R

doi:10.1097/00006254-198503000-00004

Cited by 30 publications

(36 citation statements)

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“…Hustin et al 32 and Meekins et al 19 reported findings on cytotrophoblast (CTB) invasion (for findings and limitations, see online-only Data Supplement).…”

Section: Endovascular Trophoblastmentioning

confidence: 99%

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Spiral Artery Remodeling and Trophoblast Invasion in Preeclampsia and Fetal Growth Restriction

Lyall

Robson²,

Bulmer³

2013

Hypertension

389

250

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Failure to transform uteroplacental spiral arteries is thought to underpin disorders of pregnancy, including preeclampsia and fetal growth restriction (FGR). In this study, spiral artery remodeling and extravillous-cytotrophoblast were examined in placental bed biopsies from normal pregnancy (n=25), preeclampsia (n=22), and severe FGR (n=10) and then compared with clinical parameters. Biopsies were immunostained to determine vessel wall integrity, extravillous-cytotrophoblast location/density, periarterial fibrinoid, and endothelium. Muscle disruption was reduced in myometrial spiral arteries in preeclampsia ( P =0.0001) and FGR ( P =0.0001) compared with controls. Myometrial vessels from cases with birth weight <5th percentile ( P <0.001), abnormal uterine Doppler ( P <0.01), abnormal umbilical artery Doppler ( P <0.001), and preterm delivery ( P <0.001) had less muscle destruction compared with >5th percentile. Fewer extravillous-cytotrophoblast surrounded both decidual and myometrial vessels in the normal group and preeclampsia group compared with the FGR group ( P =0.001). For myometrial vessels, the normal group contained more intramural extravillous-cytotrophoblast than in preeclampsia ( P =0.015). Decidual vessels in the FGR group had less fibrinoid deposition compared with controls ( P =0.013). For myometrial vessels, less fibrinoid was deposited in both the preeclampsia group ( P =0.0001) and the FGR group ( P =0.01) when compared with controls, and less fibrinoid was deposited in the preeclampsia group when compared with FGR group ( P <0.001). Myometrial vessels obtained from birth weights <5th percentile had less periarterial fibrinoid than those with >5th percentile ( P <0.02). A major defect in myometrial spiral artery remodeling occurs in preeclampsia and FGR that is linked to clinical parameters. Interstitial extravillous-cytotrophoblast is not reduced in preeclampsia but is increased in FGR.

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“…Hustin et al 32 and Meekins et al 19 reported findings on cytotrophoblast (CTB) invasion (for findings and limitations, see online-only Data Supplement).…”

Section: Endovascular Trophoblastmentioning

confidence: 99%

“…Hustin et al [32] reported that "Cytotrophoblast vascular invasion which was evident up to the myometrial junction appeared to be reduced in preeclampsia and normotensive fetal growth retardation cases". No trophoblast specific antibodies were used.…”

Section: What Is New?mentioning

confidence: 99%

Spiral Artery Remodeling and Trophoblast Invasion in Preeclampsia and Fetal Growth Restriction

Lyall

Robson²,

Bulmer³

2013

Hypertension

389

250

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“…There is conflicting evidence on the deposition of C components in decidual vessels in normal and pathologic pregnancies (Hustin et al, 1983;Kitzmiller et al, 1981;Wells et al, 1987). We have re-examined this issue looking in particular at the presence of C components on DECs in view of the special interaction of these cells with endovascular trophoblast resulting in their partial replacement.…”

Section: C1q Is Localized On Decsmentioning

confidence: 99%

Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium

Bulla

Agostinis

Bossi

et al. 2008

Molecular Immunology

113

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This study was prompted by the observation that decidual endothelial cells (DECs), unlike endothelial cells (ECs) of blood vessels in normal skin, kidney glomeruli and brain, express surface-bound C1q in physiologic pregnancy. This finding was unexpected, because deposits of C1q are usually observed in pathologic conditions and are associated with complement activation. In the case of DECs, we failed to detect immunoglobulins and C4 co-localized with C1q on the cell surface. Surprisingly, DECs expressed mRNA for the three chains of C1q and secreted detectable level of this component in serum-free medium. The ability to synthesize C1q is acquired by DECs during pregnancy and is not shared by ECs obtained from endometrium and from other sources. Cell-associated C1q has a molecular weight similar to that of secreted C1q and is released from DECs following treatment with heparinase or incubation at low pH. This suggests that C1q binds to DECs and it is not constitutively expressed on the cell surface. C1q is localized at contact sites between endovascular trophoblast and DECs and acts as an intercellular molecular bridge because adhesion of endovascular trophoblast to DECs was inhibited by antibodies to C1q and to a receptor recognizing its globular portion expressed on trophoblast.

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“…1975) that decidual segments of thc uteroplacental arteries in the placental bed, having undergone physiological changes, are relatively immune from acute atherosis and the apparently contradicting findings of acutc atherosis in decidual segments (Hertig 1945;Sexton et al 1950;Zeek & Assali 1950;Kitzmiller & Benirschke 1973;Kitzmiller et ul. 1981;Sheppard & Bonnar 1976, 1981Hustin et al 1983) can now be explained. The new finding of unaltered spiral arteries throughout their course from their origin from the radial arteries to the openings in the intervillous space will reconcile the opposing views.…”

Section: O R R E S P O N D E N C Ementioning

confidence: 79%

Inadequate maternal vascular response to placentation in pregnancies complicated by preeclampsia and by small‐for‐gestational‐age infants

Labarrere

Althabe

1987

BJOG

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Maternal Vascular Lesions in Pre-eclampsia and Intrauterine Growth Retardation

Cited by 30 publications

References 0 publications

Spiral Artery Remodeling and Trophoblast Invasion in Preeclampsia and Fetal Growth Restriction

Spiral Artery Remodeling and Trophoblast Invasion in Preeclampsia and Fetal Growth Restriction

Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium

Inadequate maternal vascular response to placentation in pregnancies complicated by preeclampsia and by small‐for‐gestational‐age infants

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