The activity of the NK cells in patients with preeclampsia was studied to investigate the pathogenesis of preeclampsia. By using MTT and 51Cr releasing technique, the proliferation and killing ability of the NK cells in maternal and umbilical blood from preeclampsia patients (n = 18) and normal third trimester pregnant women (n = 18) were detected. The NK-92 cell line was as the positive control. The results showed that the NK cell counts of umbilical blood in preeclampsia patients and normal third trimester pregnant women were significantly greater than those of maternal blood (both P<0.05). Compared with that in normal third trimester pregnant women, the proliferative ability of the NK cells in preeclampsia patients was apparently increased (P<0.05). Compared with that in maternal blood, the proliferative ability of the NK cells in umbilical blood from both preeclampsia patients and normal third trimester pregnant women was dramatically increased. The killing ability of the NK cells in preeclampsia patients was significantly higher than that in normal third trimester pregnant women (P <0.05). It was suggested that both number and function of the NK cells in preeclampsia women were increased, and that in umbilical blood was greater than that in maternal blood, speculating that the function of the NK cells may affect the maintenance of the maternal and fetal immune tolerance during pregnancy.
Cytotoxicity, Immunologic/*immunology ; Fetal Blood/cytology ; Immune Tolerance ; Killer Cells, Natural/*immunology ; Killer Cells, Natural/pathology ; Pre-Eclampsia/blood ; Pre-Eclampsia/*immunology ; Pregnancy Trimester, Third

OBJECTIVE: To investigate the invason of trophoblasts in the placenta bed and the change of spiral arteries and microvessels in pre-eclampsia and normal pregnancy. METHODS: Twenty cases of normal pregnancies, mild pre-eclampsia and severe pre-eclampsia were chosen as Group A, Group B, and Group C. HE staining and immunohistochemistry staining (SP method) were used to observe the depth and the density of trophoblasts invading the placenta bed and the change of spiral arteries and microvessels. RESULTS: The significant difference in the degree of invasion was in the superficial myometrial segment. Group C was the most superficial in the 3 groups (P<0.01). The density of trophoblasts which invaded the placenta bed in the lower half of the basal decidual segment and the myometrial segment showed us Group C was the lowest (P<0.01). There was statistical difference among the 3 groups (P<0.01). The average lumen area of the spiral arteries in the decidual segment and the superficial myometrial segment of the placenta bed was the smallest in Group C among the 3 groups(P<0.01) and there was statistical difference among the 3 groups (P<0.01). The spiral arteries were the thickest in Group C with statistical difference among the 3 groups (P<0.01). The physiological and pathological change of the spiral arteries was mainly in the superficial myometrial segment. The incidence rate of physiological changes in the spiral arteries was the lowest in Group C with statistical difference among the 3 groups (P<0.01). The incidence rate of pathological changes was the highest in Group C (P<0.01) and the normal group was the highest. There was significant difference among the 3 groups(P<0.01). There was positive correlation between the physiological change of the spiral arteries and the invaing degree of the trophoblasts (P<0.05), there was negative correlation between the pathological change of the spiral arteries and the invasion depth as well as the invasion density of the trophoblasts(P<0.05). There was negative correlation between the physiological change and the pathogenetic condition of pre-eclampsia(P<0.05)while there was positive correlation between the pathological change and the pathogenetic condition degree of pre-eclampsia(P<0.05). There was negative correlation between the invasion depth as well as density in uteruso superficial myometrial segment by trophoblast and the pathogenetic condition degree of pre-eclampsia(P<0.05). There was invasion trophoblast in 62.50% lumen wall of spiral arteries in uterus superficial myometrial segment of the placental bed in normal pregnancy while 27.5% was seen in severe pre-eclampsia. Microvascular density in the decidual segment and the superficial myometrial segment of the placenta bed in Group C was the lowest among the 3 groups with statistical difference (P<0.01). CONCLUSION The invasion depth of the trophoblasts in pre-eclampsia was more superficial than normal pregnancy.The changes of the invasion of the trophoblasts and the pathological changes of the spiral arteries in the placenta bed mainly existed in the superficial myometrial segment which was closely related to the severity of the illness. That microvascular density in the placental bed of pre-eclampsia started to decrease from the basal decidual segment shows that the microvessel development in the placenta bed is impaired in pre-eclampsia.
Adult ; Arteries ; pathology ; Capillaries ; pathology ; Female ; Humans ; Placenta ; blood supply ; pathology ; Pre-Eclampsia ; pathology ; Pregnancy ; Trophoblasts ; pathology

OBJECTIVETo explore the pathologic features and prognosis of early and late onset severe preeclampsia.

METHODSAn observational study was conducted in 178 cases of severe preeclampsia collected during January 2010 to December 2014 from Haidian Maternal and Child Health Hospital.The cases were divided into two groups according to the onset of gestational age of the severe preeclampsia, with 54 cases of namely early onset (onset ≤ 34 weeks) and 124 cases of late onset (onset >34 weeks). Clinical characteristics of the patients, perinatal outcome and the pathologic characteristics of the placentas in each group were evaluated.

RESULTSDecidual vascular disease, placental infarction, abruptio placentae and placental villi dysplasia were seen in both groups. The incidence of placental villi dysplasia was the highest, followed by placental infarction. Incidence of severe decidual vascular disease of early and late onset severe decidual vascular disease were 16.7% (9/54) and 5.6% (7/124), respectively.Incidence of placental infarction of early and late onset severe preeclampsia were 48.1% (26/54) and 61.3% (76/124). Incidence of placental villi dysplasia of early and late onset severe preeclampsia were 79.6% (43/54) and 50.8% (63/124). Incidence of Severe decidual vascular disease, placental infarction and placental villi dysplasia were significantly different between early and late onset severe preeclampsia cases (P<0.05), while there was no difference in decidual vascular disease and placenta thrombi (P>0.05). Fetal survival rate of every group was 81.5% (44/54) and 93.5% (116/124). Incidence of fetal growth retardation was 55.6% (30/54) and 38.7% (48/124). The fetal survival rate and incidence of fetal growth retardation were different between two groups (P<0.05).

CONCLUSIONSThe incidence of decidual vascular disease and placental villi dysplasia in early onset severe preeclampsia is higher than those in late onset severe preeclampsia. Neonatal outcome and prognosis in early onset severe preeclampsia are worse than those in late onset severe preeclampsia.

Chorionic Villi ; pathology ; Female ; Fetus ; Gestational Age ; Humans ; Placenta ; pathology ; Placenta Diseases ; epidemiology ; pathology ; Pre-Eclampsia ; epidemiology ; pathology ; Pregnancy

The mechanism of apoptosis was first discovered at the end of the 19th century, but it was only recently that its importance was recognized. Not only in a pathologic environment but also in a normal environment, apoptosis has an important role in homeostasis. The number of cells is restricted by apoptosis which is controlled by several SlgBS lll VlVO. In pregnancy, the placenta regulates the maternal-fetal exchange of molecules and functions as a barrier for the protection of the fetus. As the pregnancy proceeds, changes occur in the number and components of placental cells. Observing the placental tissues, apoptosis was found in the syncytiotrophoblasts of early and late pregnancy. In particular, the fact that apoptosis observed in the placenta of late pregnancy supports the hypothesis that pmgrammed cell death is a normal sequence. Pregnancy-induced hypertension is usually accompanied by abnormal placenta and intrauterine growth restriction. In this study, using the TdT-FragEL DNA fragmentation detection kit, the changes in the nucleus by apoptosis in the placental tissues of 23 to 40 gestational weeks in preeclampsia and eclampsia were compared with normal placenta. Apoptosis was observed in the normal term placenta and in pregnancy-induced hypertension patients, regardless of whether vasculopathy was observed in Doppler ultrasound or confirmed by pathology, more apoptoses were observed aside from the number of gestational weeks.
Apoptosis ; Cell Death ; DNA Fragmentation ; Eclampsia ; Female ; Fetus ; Homeostasis ; Humans ; Hypertension, Pregnancy-Induced* ; Maternal-Fetal Exchange ; Pathology ; Placenta* ; Pre-Eclampsia ; Pregnancy ; Trophoblasts ; Ultrasonography

OBJECTIVETo investigate the expression of annexin V in the decidua tissues of preeclampsia patients and explore its clinical significance.

METHODSReal-time PCR, Western blotting and immunohistochemistry were employed to detect the mRNA and protein expressions of annexin V in the deciduas from 35 normal pregnant women at full term, 38 early onset severe preeclampsia patients and 33 late onset severe preeclampsia patients.

RESULTSAnnexin V was found on the cell membrane and in the cytoplasm of the decidual cells and stroma. Both the mRNA and protein of annexin V expressions in the decidua tissues were significantly different between normal pregnancy group and early or late onset severe preeclampsia group (P<0.05), being the highest in normal pregnancy group and the lowest in early onset severe preeclampsia group.

CONCLUSIONThe low expression of annexin V in the deciduas might participate in the hypercoagulability state in preeclampsia patients.

Adult ; Annexin A5 ; metabolism ; Case-Control Studies ; Decidua ; metabolism ; Female ; Humans ; Immunohistochemistry ; Pre-Eclampsia ; metabolism ; pathology ; Pregnancy ; RNA, Messenger ; genetics

Preeclampsia and intrauterine growth restriction (IUGR) of the fetus are the two most common pregnancy complications worldwide, affecting 5%-10% of pregnant women. Preeclampsia is associated with significantly increased maternal and fetal morbidity and mortality. Hypoxia-induced uteroplacental dysfunction is now recognized as a key pathological factor in preeclampsia and IUGR. Reduced oxygen supply (hypoxia) disrupts mitochondrial and endoplasmic reticulum (ER) function. Hypoxia has been shown to alter mitochondrial reactive oxygen species (ROS) homeostasis and induce ER stress. Hypoxia during pregnancy is associated with excessive production of ROS in the placenta, leading to oxidative stress. Oxidative stress occurs in a number of human diseases, including high blood pressure during pregnancy. Studies have shown that uterine placental tissue/cells in preeclampsia and IUGR show high levels of oxidative stress, which plays an important role in the pathogenesis of both the complications. This review summarizes the role of hypoxia-induced mitochondrial oxidative stress and ER stress in the pathogenesis of preeclampsia/IUGR and discusses the potential therapeutic strategies targeting oxidative stress to treat both the pregnancy complications.
Pregnancy ; Female ; Humans ; Placenta ; Fetal Growth Retardation/etiology* ; Pre-Eclampsia/pathology* ; Reactive Oxygen Species ; Hypoxia/pathology* ; Pregnancy Complications/pathology* ; Endoplasmic Reticulum Stress

BACKGROUNDEarly and late-onset preeclampsia is thought to be different disease entities. This study aimed to determine the effects of early-onset preeclampsia-like symptoms on feto-placental outcomes and the adverse impacts of various factors on placental and fetal growth and development at different gestational stages in a mouse model.

METHODSPregnant C57BL/6J mice were divided into control and preeclampsia (PE) groups, and injected subcutaneously with the nitric oxide synthase inhibitor L-arginine methyl ester (L-NAME) 50 mgxkg(-1)d(-1). The PE group was divided into early-, mid- and late-PE groups with L-NAME injections starting on days 7, 11 and 16 of pregnancy, respectively. Corresponding control groups were injected with saline at the same time points. Blood pressure was measured until days 14 and 18, when the fetuses and placentas were removed under anesthesia. Blood pressure, urinary protein, and fetal and placental conditions were analyzed.

RESULTSBlood pressure and urinary protein increased following L-NAME injection. The fetal survival rate and fetal weight were reduced and the fetal absorption rate was increased in the early-PE group on days 14 and 18 of pregnancy, compared with the control group. There were no significant differences in these parameters between the late-PE group and the respective control group. Placental weights in the early- and mid-PE groups were significantly reduced at days 14 and 18 of pregnancy compared with the control groups, but there was no significant difference in placental weight between the late-PE group and the respective control group. Morphologic examination of placentas from the early- and mid-PE groups showed varying degrees of fibrinoid necrosis and villous interstitial edema, but no significant pathologic changes were found in the placentas from the late-PE or control groups.

CONCLUSIONPreeclampsia-like symptoms occurring during the early stage of pregnancy are more likely to affect placental and fetal development, whereas late onset preeclampsia-like symptoms have a direct impact on the mothers.

Animals ; Blood Pressure ; Disease Models, Animal ; Female ; Fetal Development ; Fetal Resorption ; etiology ; Fetal Weight ; Mice ; Mice, Inbred C57BL ; Organ Size ; Placenta ; pathology ; Pre-Eclampsia ; pathology ; physiopathology ; Pregnancy

BACKGROUND: Histologic examination of the placentas from intrauterine growth retardation (IUGR) fetuses can supplement clinical knowledge of the cause of IUGR. The present study was undertaken to observe the pathologic findings regarding the placentas in IUGR fetuses. METHODS: Clinicopathologic findings in 45 cases with IUGR at the third-trimester were reviewed, and they were compared with those of 24 normal control cases. An IUGR fetus was defined as one with a birth weight less than those in the 10th percentile. Of the IUGR cases, 15 were hypertensive IUGR with or without preeclampsia, and 30 were normotensive IUGR. RESULTS: The IUGR groups had significantly shorter mean gestational ages, lower mean placental weights, and higher incidences of oligohydramnios, compared to the normal controls (p<0.05). Histologically, IUGR was characterized by increased incidence of decidual vasculopathy (31.1%, p<0.05), multiple and severe infarct (p<0.05), villous fibrosis (31.1%, p<0.05), syncytiotrophoblastic knots (86.7%, p<0.05), and higher degree of increased perivillous fibrin deposition (p<0.05). However, there were no statistically significant differences in the placental lesions between hypertensive and normotensive IUGR cases, except for the presence of decidual vasculopathy. CONCLUSIONS: Abnormal uteroplacental vasculature and chronic uteroplacental insufficiency, coagulation-related pathology in the uteroplacental, intervillous and/or fetoplacental vasculature, and chronic inflammatory lesions may be the primary disease processes related to the placental pathology of IUGR. Although the cause of IUGR pregnancies is heterogeneous, careful cilinicopathologic correlations in individual cases are necessary in the interpretation of placental lesions of IUGR, and the total burden of several placental lesions may be more important than a single histologic feature.
Birth Weight ; Female ; Fetal Growth Retardation* ; Fetus ; Fibrin ; Fibrosis ; Gestational Age ; Incidence ; Oligohydramnios ; Pathology* ; Placenta ; Pre-Eclampsia ; Pregnancy ; Trophoblasts ; Weights and Measures

The activity of the NK cells in patients with preeclampsia was studied to investigate the pathogenesis of preeclampsia. By using MTT and 51Cr releasing technique, the proliferation and killing ability of the NK cells in maternal and umbilical blood from preeclampsia patients (n = 18) and normal third trimester pregnant women (n = 18) were detected. The NK-92 cell line was as the positive control. The results showed that the NK cell counts of umbilical blood in preeclampsia patients and normal third trimester pregnant women were significantly greater than those of maternal blood (both P<0.05). Compared with that in normal third trimester pregnant women, the proliferative ability of the NK cells in preeclampsia patients was apparently increased (P<0.05). Compared with that in maternal blood, the proliferative ability of the NK cells in umbilical blood from both preeclampsia patients and normal third trimester pregnant women was dramatically increased. The killing ability of the NK cells in preeclampsia patients was significantly higher than that in normal third trimester pregnant women (P <0.05). It was suggested that both number and function of the NK cells in preeclampsia women were increased, and that in umbilical blood was greater than that in maternal blood, speculating that the function of the NK cells may affect the maintenance of the maternal and fetal immune tolerance during pregnancy.
Adult ; Cytotoxicity, Immunologic ; immunology ; Female ; Fetal Blood ; cytology ; Humans ; Immune Tolerance ; Killer Cells, Natural ; immunology ; pathology ; Pre-Eclampsia ; blood ; immunology ; Pregnancy ; Pregnancy Trimester, Third

OBJECTIVETo investigate the level of hypermethylated ras association domain family 1A (RASSF1A) gene in maternal plasma of pre-eclampsia and its clinical value.

METHODSSixty pre-eclampsia women including 30 mild and 30 severe cases were selected, 60 women with normal pregnancy were studied as control. Free DNA from plasma samples was extracted, fluorescence quantitative polymerase chain reaction (FQ-PCR) was used to detect the concentrations of RASSF1A gene before and after methylation-sensitive restriction digestion. Meanwhile, beta-actin gene was detected as a control to confirm complete enzyme digestion.

RESULTSThe median concentration of hypermethylated RASSF1A gene was 3.31-fold higher in samples from pre-eclamptic pregnancies than that in controls. There was significant difference between the mild and severe pre-eclamptic subjects (P<0.05), with the median concentrations of 1659 copies/mL and 2036.50 copies/mL, respectively.

CONCLUSIONHypermethylated RASSF1A gene in pre-eclampsia plasma was significantly increased and the concentrations were related to the severity of pre-eclampsia.

Adult ; DNA ; blood ; metabolism ; DNA Methylation ; Female ; Humans ; Pre-Eclampsia ; genetics ; metabolism ; pathology ; Pregnancy ; Tumor Suppressor Proteins ; genetics ; metabolism ; Young Adult