Monocytes are increased in pregnancy after gestational hypertensive disease

Abstract

Monocytes derive from bone marrow and circulate in the blood. They phagocytose, produce cytokines and present antigens. Individual monocyte subsets play distinct roles in the pathogenesis of cardiovascular disease, but their implications in gestational hypertensive disease are unclear. Our objective was to examine the difference in monocyte subsets between pregnant women with or without previous hypertension in pregnancy. Women were enrolled in a prospective observational study in which monoclonal antibodies against cell surface receptors were used to detect monocytes in the peripheral blood by flow cytometry. We compared 17 pregnant women with previous hypertension in pregnancy (Group 1) and 42 pregnant women without previous gestational hypertensive disease (Group 2) with 27 healthy, non-pregnant controls (Group 3). The pregnant women were studied at 13 ± 1 weeks gestation. Monocyte subsets were quantified by flow cytometry: Mon1 (CD14++CD16-CCR2+), Mon2 (CD14++CD16+CCR2+), Mon3 (CD14+CD16+CCR2-), their aggregates with platelets and expression of the surface markers. The groups were well-matched for age, body mass index and ethnicity (P > 0.05 for all). Mon1 counts were higher in women with a history of gestational hypertension or preeclampsia compared to other groups (Group 1 = 441 per µl (376–512); Group 2 = 357 (309–457); Group 3 = 323 (277–397); P < 0.001). Mon3 was higher in both groups of pregnant women compared to non-pregnant controls (Group 1 = 51 (38–62); Group 2 = 38 (29–58); Group 3 = 26 (20–40), P = 0.002). Increased monocytes in women with a previous hypertensive pregnancy generates a hypothesis that these cells may link hypertension in pregnancy, chronic inflammation and future cardiovascular risk.

Pathway-enhanced Transformer-based robust model for quantifying cell types of origin of cell-free transcriptome

“…Among fetal cells, the fractions of mesencephalon and hepatocyte cells increased significantly with gestation, while cardiomyocyte cells significantly decreased, and there was no significant change in the fractions of kidney epithelial cells. In the early-onset pre-eclampsia (PE) group, Deconformer showed significantly higher contributions of endothelial cell, kidney epithelial cell, smooth muscle cell, hepatocyte, monocyte[46] compared to the control group, consistent with the symptoms of proteinuria, impaired hepatocyte function, renal insufficiency, and increased blood pressure in early-onset PE patients[43] (Fig. 3E), and an increased contribution of platelets, possibly related to thrombocytopenia in early-onset PE patients.…”