Antigenic identification of cells in spiral artery trophoblastic invasion: Validation of histologic studies by triple-antibody immunocytochemistry

Labarrere, Carlos A.; Faulk, W. Pagé

doi:10.1016/0002-9378(94)90464-2

Cited by 25 publications

(14 citation statements)

References 19 publications

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“…We also examined fetal trophoblasts in decidual sections showing AGT signal in vessels by in situ RT-PCR. We confirmed that trophoblasts were present in the section by staining serial sections for low molecular weight cytokeratin (43).…”

Section: Methodssupporting

confidence: 59%

Angiotensinogen T235 expression is elevated in decidual spiral arteries.

Morgan¹,

Craven²,

Nelson³

et al. 1997

J. Clin. Invest.

108

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Preeclampsia is associated with a common molecular variant of angiotensinogen (Met235Thr). This variant is in tight linkage disequilibrium with a mutation in the angiotensinogen promoter, G( Ϫ 6)A, which leads to elevated expression in vitro. Since angiotensin II levels could play a role in atherotic changes of the uterine spiral arteries associated with preeclampsia, we investigated angiotensinogen expression in the first trimester uterus. We localized angiotensinogen transcription in uterine decidua using in situ reverse transcription PCR. We then compared decidual T235 expression levels to M235 levels in heterozygous women using an allele-specific ligation assay and a single nucleotide primer extension assay. In human decidua, angiotensinogen is expressed only in spiral artery smooth muscle cells. Heterozygous women have significantly elevated expression of the T235 allele compared to the M235 allele ( P Ͻ 0.0001). These observations suggest that elevated expression of the T235 allele in decidual spiral arteries may cause first trimester atherotic changes leading to preeclampsia. ( J. Clin.

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Section: Methodssupporting

confidence: 59%

Angiotensinogen T235 expression is elevated in decidual spiral arteries.

Morgan¹,

Craven²,

Nelson³

et al. 1997

J. Clin. Invest.

108

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“…Finally, the frequency of atherosis in our study was higher than the frequency recently described in a large population of placentas from normal and abnormal pregnancies [159,162]. We believe this is due to the high sensitivity of triple-antibody immunohistochemistry when compared with hematoxylin-eosin used to detect failure of physiologic transformation of the spiral arteries and placental atherosis [44]. …”

Section: Commentcontrasting

confidence: 58%

“…Sample slides having basal plate spiral arteries defined immunohistochemically were included in the study, and samples without any spiral artery were excluded. A triple-antibody technique [44,73] with antibodies to α-smooth muscle actin to identify vascular smooth muscle cells, cytokeratin to identify extravillous trophoblasts and intra-arterial trophoblasts, and von Willebrand factor to identify endothelial cells was used to detect complete or partial failure of physiologic transformation and physiologic transformation of spiral arteries (median of 4 [minimum: 1; maximum: 9] vessels per placental basal plate). A triple-antibody immunohistochemistry with α-actin, cytokeratin, and ICAM-1 identified interstitial extravillous trophoblast and spiral artery endothelial cell activation [44,73,91].…”

Section: Methodsmentioning

confidence: 99%

“…This has practical implications because the basal plate of the placenta is available for examination in all cases while a placental bed biopsy requires a specialized procedure generally performed during a cesarean delivery. Immunohistochemistry [44] allows in-depth examination of the vessel wall through antigen detection of its different cellular components, which reduces the subjectivity of using only conventional light microscopy for vessel recognition in the placental basal plate.…”

Section: Introductionmentioning

confidence: 99%

“…Women with preeclampsia, the prototypic obstetrical complication characterized by failure of physiologic transformation of the spiral arteries [19,21,32,54–58] have evidence of intravascular inflammation [57,59–62] as well as changes in lipid metabolism [63–66], such as increased concentrations of triglycerides, and low-density lipoprotein, and decreases in low-density lipoprotein particle size and high-density lipoprotein [67]. Macrophage infiltration of the intima and media is identified in both atherosis and the lesions found in transplant vasculopathy [6,43,44,58,68–70]. Therefore, there are striking parallels between preeclampsia and atherosclerosis, as well as the lesions of atherosis and those observed in patients with ischemic heart disease.…”

Section: Introductionmentioning

confidence: 99%

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Failure of physiologic transformation of spiral arteries, endothelial and trophoblast cell activation, and acute atherosis in the basal plate of the placenta

Labarrere

DiCarlo

Bammerlin

et al. 2017

American Journal of Obstetrics and Gynecology

Self Cite

131

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Background Failure of physiologic transformation of spiral arteries has been reported in preeclampsia, fetal growth restriction, fetal death, and spontaneous preterm labor with intact or ruptured membranes. Spiral arteries with failure of physiologic transformation are prone to develop atherosclerotic-like lesions of atherosis. There are striking parallels between preeclampsia and atherosclerotic disease, and between lesions of atherosis and atherosclerosis. Endothelial activation, identified by intercellular adhesion molecule-1 expression, is present in atherosclerotic-like lesions of heart transplantation and considered a manifestation of rejection. Similarly, endothelial activation/dysfunction has been implicated in the pathophysiology of atherosclerosis and preeclampsia. Intercellular adhesion molecule-1-overexpressing-activated endothelial cells are more resistant to trophoblast displacement than nonactivated endothelium and may contribute to shallow spiral artery trophoblastic invasion in obstetrical syndromes having failure of physiologic transformation. Objective To determine whether failure of spiral artery physiologic transformation was associated with activation of interstitial extravillous trophoblasts and/or spiral artery endothelium and presence of acute atherosis in the placental basal plate. Study Design A cross-sectional study of 123 placentas (19-42 weeks’ gestation) obtained from normal pregnancies (n = 22), preterm prelabor rupture of membranes (n = 26), preterm labor (n = 23), preeclampsia (n = 27), intrauterine fetal death (n = 15), and small for gestational age (n = 10) was performed. Failure of spiral artery physiologic transformation and presence of cell activation was determined using immunohistochemistry of placental basal plates containing a median of 4 (minimum: 1; maximum: 9) vessels per placenta. Endothelial/trophoblast cell activation was defined by the expression of intercellular adhesion molecule-1 (ICAM-1). Investigators examining microscopic sections were blinded to clinical diagnosis. Pairwise comparisons among placenta groups were performed with the Fisher’s exact and Wilcoxon rank sum tests using a Bonferroni-adjusted level of significance (.025). Results 87% (94/108) of placentas having spiral arteries with failure of physiologic transformation (actin-positive and cytokeratin-negative) in the basal plate, and 0% (0/15) of placentas having only spiral arteries with complete physiologic transformation (cytokeratin-positive and actin-negative), had arterial endothelial and/or interstitial extravillous trophoblasts reactive with the ICAM-1 activation marker (P < .001). A significant correlation (R2 = 0.84) was found between expression of spiral artery endothelial and interstitial extravillous trophoblast ICAM-1 (P < .001) in activated placentas. Lesions of atherosis were found in 31.9% (30/94) of placentas with complete and/or partial failure of physiologic transformation of spiral arteries that were ICAM-1-positive, in none of the 14 placentas with failure of physiolog...

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