Syncytiotrophoblast intercellular adhesion molecule-1 expression in placental villitis of unknown cause

Labarrere, Carlos A.; Ortíz, Miguel A; Sosa, M.J.; Campaña, Gonzalo; Wernicke, Mario; Baldridge, Lee Ann; Terry, Colin; DiCarlo, Hector L.

doi:10.1016/j.ajog.2004.12.090

Cited by 19 publications

(9 citation statements)

References 22 publications

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“…Local activation of platelets, coagulation components, or complement by antiphospholipid or other antibodies might lead to necrosis of syncytiotrophoblast. Second, although syncytiotrophoblast does not usually express adhesion molecules, it can be induced to express intercellular adhesion molecule 1 in cases of VUE [44]. Other evidence suggests that E-selectin can be induced on villous trophoblast by lipopolysaccharide [45].…”

Section: Access To Fetal Tissuesmentioning

confidence: 95%

Villitis of unknown etiology: noninfectious chronic villitis in the placenta

2007

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Section: Access To Fetal Tissuesmentioning

confidence: 95%

Villitis of unknown etiology: noninfectious chronic villitis in the placenta

2007

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“…Macrophages inhibit extravillous trophoblast invasion both passively, by being attracted by extravillous trophoblasts, and actively, by inducing peri-arterial extravillous trophoblast apoptosis [152]. Arterial ICAM-1 up-regulation could facilitate macrophage recruitment as shown in placental villitis of unknown etiology and massive chronic intervillositis [153,154]. Aberrant ICAM-1 expression has been described in cultured syncytiotrophoblasts pre-treated with both inflammatory cytokines, which also facilitate adhesion of monocytes to the syncytiotrophoblast [155].…”

Section: Commentmentioning

confidence: 99%

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

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130

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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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“…Both Class I and Class II MHC antigens are absent from normal syncytiotrophoblast , but in VUE lesions, segments of syncytiotrophoblast membrane react to antibodies against Class II antigens , including HLA‐DR, HLA‐DP, and HLA‐DQ , which may be the result of cytokine signaling by activated fetal macrophages . Abnormally increased intercellular adhesion molecule 1 (ICAM‐1) expression has been described on syncytiotrophoblast , which would facilitate traffic of maternal immune cells into villi, but the reason for such upregulation is unclear. Maternal rejection of the fetoplacental unit also is supported observations such as increased rates of VUE when in vitro fertilization pregnancies utilize donor rather than native oocytes .…”

Section: Villitis Of Unknown Etiologymentioning

confidence: 99%

Placental pathologic lesions with a significant recurrence risk – what not to miss!

Chen

Roberts

2017

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Here, we review three important placental pathologies with significant clinical implications and recurrence risks. They are, in order of most to least frequently seen, villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition (also known as maternal floor infarction). These entities occur in both preterm and term gestations and are observed more frequently with maternal and obstetric disorders including prior pregnancy loss, hypertension/preeclampsia, and autoimmune disease. They are associated with, and probably the cause of, significant perinatal morbidity and mortality including intrauterine growth restriction, fetal and neonatal demise, and fetal/neonatal neurocompromise (seizures and cerebral palsy). All three entities have high recurrence risks, with recurrence rates ranging from 34 to 100%. The histologic features of villitis of unknown etiology, chronic histiocytic intervillositis, and massive perivillous fibrin deposition are described herein. We discuss the clinical associations and suggest the subsequent clinical and pathological evaluation. Hypotheses as to the biology of these lesions are reviewed.

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Syncytiotrophoblast intercellular adhesion molecule-1 expression in placental villitis of unknown cause

Cited by 19 publications

References 22 publications

Villitis of unknown etiology: noninfectious chronic villitis in the placenta

Villitis of unknown etiology: noninfectious chronic villitis in the placenta

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

Placental pathologic lesions with a significant recurrence risk – what not to miss!

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