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Uteroplacental atherosis: The atherosclerosis of the placenta.
Author(s) -
Labarrere Carlos Alberto,
DiCarlo Hector L.,
Hardin James W.,
Kim Yeon M.,
Erez Offer,
Kassab Ghassan S.,
Romero Roberto
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.03770
Subject(s) - spiral artery , placenta , preeclampsia , medicine , andrology , umbilical artery , fetus , lesion , gestational age , pregnancy , pathology , biology , genetics
Background and Objective Fetal growth during pregnancy is directly related to the transformation of spiral arteries of the placental bed into uteroplacental arteries (physiologic conduits containing endothelial cells and trophoblastic cells embedded in fibrinoid deposits that replace the smooth muscle cell layer). Failure of physiologic transformation of the spiral arteries leads to development of uteroplacental atherosis (UA), a lesion similar to native atherosclerosis ( native atherosis ). Our objective was to evaluate UA cell composition, variations in cell composition among obstetrical syndromes, and evidence of activation and inflammation in the lesions. Methods Basal plate samples (5.6 ± 0.9/placenta) from placentas with (n=134) and without (n=134) UA were studied histo and immunohistochemically for different cell types. Statistical comparisons for UA and no UA groups were performed with Fisher’s exact, Kruskal‐Wallis, Wilcoxon Rank Sum test, and analysis of variance (ANOVA); and a Bonferroni‐adjusted level of significance of <0.025 was used. Results All 134 placentas with UA had failure of spiral artery physiologic transformation (total and/or partial); 125 (93.3%) being from complicated pregnancies, and 9 (6.7%) from normal pregnancies. UA was found in small for gestational age (n=31), preeclampsia (n=73), preterm labor (n=8), preterm pre‐labor rupture of membranes (n=9), fetal death (n=4) and adequate for gestational age (n=9) placentas. UA had 52.4% smooth muscle cells, 29.4% foam cells, 30.6% oil red O‐positive cells, 16.2% endothelial cells and 0% intra‐arterial trophoblast cells; failure of physiologic transformation had 82.2% smooth muscle cells, 17.0% endothelial cells, 0% foam cells, 0% oil red O‐positive cells and 0% intra‐arterial trophoblast cells; physiologic transformation had 81.0% intra‐arterial trophoblast cells, 17.6% endothelial cells, 0% foam cells, 0% oil red O‐positive cells and only 0.4% smooth muscle cells. UA lesions were 100% fibrin‐positive and had 31.5% CD68‐ and 30.8% CD36‐positive macrophages within the fibrin matrix; while arteries with failure of physiologic transformation and with physiologic transformation had no fibrin and less than 1% CD68‐ and CD36‐positive macrophages. UA had 48.0–48.9% ICAM‐1‐, HLA‐DR‐ and NFκB‐positive cells (endothelium and macrophages), 17.4% being CRP‐reactive (predominantly proinflammatory tissue‐associated monomeric CRP); failure of physiologic transformation had 13.4–13.8% ICAM‐1‐ and HLA‐DR‐positive cells (endothelium), 7.6% of them were NFκB‐positive but none CRP‐reactive; no activation and inflammation markers were found in physiologic transformation . Conclusions We conclude that UA cell composition is the same in all obstetrical syndromes and in normal pregnancies; and UA lesions have cell activation and inflammation and oil red O‐positive CD68‐reactive macrophages containing the scavenger receptor CD36 , sharing similar characteristics with native atherosclerosis.