Placenta In Pregnancy Induced Hypertension Research Articles

Bibliometric study of placenta in pregnancy-induced hypertension

Bibliometric study of placenta in pregnancy-induced hypertension

Gross Changes of Placenta in Pregnancy Induced Hypertension and its Clinical Relevance: A Cross-sectional Study

Introduction: Placenta establishes connection between mother and foetus through umbilical cord. Pregnancy Induced Hypertension (PIH) is one of the most common complication of pregnancy. Gross study of placenta in PIH gives an insight into prenatal health of baby and mother, thereby preventing maternal as well as foetal morbidity and mortality. Aim: To study the gross changes of placenta in PIH cases with its clinical relevance. Materials and Methods: A prospective cross-sectional study was done at tertiary care hospital of Osmania and Gandhi Medical College, Telangana, India. The study was carried over for a period of six months (from October 2019 to March 2020) with a sample size of 50 placentae in PIH mothers aged between 20-35 years who were inpatients at the Obstetrics Department. They were followed until delivery. Postdelivery, the gross anatomy of the collected placentas was studied. Varied parameters of placenta, data of newborn and clinical picture of mother were compared with normal standards and statistically analysed by using Unpaired t-test. Results: Significant reduction of mean placental weight and mean foetal weight (p-value<0.0001) and significant increase in foetoplacental weight ratio was found. There was an average reduction of number of cotyledons by 23% in PIH cases when compared to normal placentae. An incidence of mean infarct areas of 9.6 and mean calcified areas of 13 were found on the maternal surface of placenta in PIH. An incidence of 68% of marginal type of placenta was observed in patients with PIH. Clinically, incidence of headache, pedal oedema, convulsions, visual disturbances and proteinuria were found. Conclusion: Gross study of placenta in PIH reflects maternal and foetal status and can be taken as confirmative evidence by radiologists to prevent Intra Uterine Growth Retardation (IUGR) and guide obstetricians during management of pregnant mother with PIH. Thereby, preventing the maternal and foetal morbidity and mortality.

Study of histological changes of placenta in pregnancy-induced hypertension in poorvanchal region of Uttar Pradesh, India

Introduction: The placenta is a fetomaternal organ. It is a connection of the fetus with the uterine wall of mother. Through the placenta, exchange of gases and nutrient supply takes place. Through the placenta, fetal blood tissue comes in direct contact with the maternal blood without any rejection. It is a special transient organ of pregnancy. In our study, we carried out the microscopic examination of the placenta in pregnancy-induced hypertension, i.e., syncytial knot, cytotrophoblastic cellular proliferation, fibrinoid necrosis, endothelial proliferation, and calcified villous spot. Material and Methods: One hundred and fifty-two placentas of full-term pregnancy were collected from the labor room/operation theater of the Gynecology and Obstetrics Department of the Government Medical College and Superfacility Hospital Azamgarh. Out of one hundred and fifty-two placentas, 76 cases were controls from mothers with no known history of preexisting hypertension and 76 were collected from mothers with pregnancy-induced hypertension. Placentas were kept in 10% formalin for 24 h for fixation. After 24 h, tissues of placentas were passed through a series of the procedures from dehydration and clearing to wax impregnation before being sectioned from automated microtome. Time took for processing was 24 h. Five microns thick tissues sections were cut. Prepared slides were mounted in DPX and covered with the cover slip. Through binocular light, microscope slides were examined at ×10, ×40, and ×100 magnifications. Results: Histology in our study revealed that syncytial knots were present in placentas of all 100% of hypertensive and only 32.89% of normotensive mothers. Cytotrophoblastic proliferation was seen in 98.68% and 19.73% placentas of hypertensive and normotensive mothers, respectively. Fibrinoid necrosis of placenta was found in 88.15% of hypertensive and only 28.94% of normotensive mothers. The 100% placentas of the hypertensive mothers had endothelial proliferation as compared to controls. Calcified villous spots were seen in 84.21% and 31.57% of placentas of hypertensive and normotensive mothers, respectively. Discussion and Conclusion: Pregnancy-induced hypertension adversely affects the health of the fetus through its harmful effects on the placentas. Syncytial knots, cytotrophoblastic cellular proliferation, fibrinoid necrosis, endothelial proliferation, and the calcified villous spots were present more in the placentas of hypertensive mothers in our study in comparison to the study of other authors. In our research, we found that endothelial proliferations were present in all placentas. If proper treatment is given to the mother in the early stage of pregnancy, it may prevent the death of a fetus. Hence, this study helps the clinician for early diagnosis and treatment of pregnancy-induced hypertension.

Morphometric differentiation between placenta in PIH and normal pregnancy

Background: Placenta is like a diary of gestational life. It is the vital organ for developing fetus, and it is also the most accessible organ of human body. Pregnancy complications such as hypertension, diabetes, and anemia are reflected in a significant way. Placental examination is helpful to plan a safe pregnancy and a healthy baby outcome at its end. Objective: To study morphometric differences of placenta in normal pregnancy and pregnancy-induced hypertension (PIH). Materials and Methods: A total of 100 placentas (50 from normal pregnancy and 50 from PIH group) were collected. Parameters such as weight, volume, thickness, diameter, and area were noted and their means were calculated. These parameters were divided into different ranges. From the weight of the baby and that of the placenta, fetoplacental weight ratio and placental coefficient were calculated. Results: The mean placental weight, area, volume, diameter, and thickness were lower in the PIH group. Weight, volume, area, diameter, and thickness in control group range from 420 to 560 g, 380 to 550 cc, 204.4 to 346 cm2, 17 to 21 cm, 1.7 to 2.3 cm, respectively, and those in PIH group range from 200 to 510 g, 190 to 500 cc, 132.7 to 247.3 cm2, 13 to 18 cm, and 1.2 to 2 cm, respectively. Conclusion: The range of morphometric parameters is comparatively lower in PIH group than in control group. The mean birth weight and fetoplacental weight ratio is higher in control group. The placental coefficient was significantly higher in PIH group.

Study of structural changes in placenta in pregnancy-induced hypertension.

Background:Hypertension is one of the most common complication during pregnancy. It contributes significantly to maternal and perinatal morbidity and mortality. This study was designed to investigate the morphological and histopathological changes in placenta from pregnancies complicated with hypertension.Objectives:To study the morbid changes in placenta in cases of pregnancy-induced hypertension (PIH) and to correlate the findings with birth weight of new born babies in comparison with normotensive mothers.Materials and Methods:The study was done on 100 placentas, out of which 50 were collected from normotensive mothers and the remaining 50 from PIH cases. All the placentas were studied morphologically and histologically. The birth weight of neonates was recorded.Results:In the present study it was observed that weight and dimensions of placenta was less in study group when compared with control group. The mean neonatal birth weight was more in normal pregnancy and feto-placental weight ratio was significantly high in hypertensive group. Histopathological study showed significant number of syncitial knots, areas of fibrinoid necrosis, hyalinization, calcification, and medial coat proliferation of medium sized blood vessels in hypertensive group.Conclusion:PIH significantly affects the placenta by reducing its weight and dimensions. These changes may cause placental insufficiency as a result of compromised utero-placental blood flow. Therefore has an adverse affect on the neonatal birth weight. PIH has definite influence on morphology, histology of placenta, and thus affects the growth of the fetus.

Immunohistochemical localization of bilirubin oxidation in human placenta

Immunohistochemical localization of bilirubin oxidation in human placenta

Expression of Angiotensin II Receptor-like 1 in the Placentas of Pregnancy-induced Hypertension

Angiotensin II receptor-like 1 (APJ), a G protein-coupled receptor that was identified as a homologue of angiotensin II type 1 (AT1) receptor, exerts antagonistic effects on AT1-mediated vasoconstriction. Studies on pregnancy-induced hypertension (PIH) revealed aberrant activation of AT1 downstream signaling. In contrast, little is known about APJ in the pathophysiology of human pregnancy. In this study, we investigated APJ expression in normal human and PIH placentas. mRNAs were extracted from 50 placental villous tissues of 18 cases with severe PIH (8 late-onset, 4 early-onset, and 6 superimposed PIH) and 32 control pregnancies (including 6 preterm cases). Histopathologic studies were conducted using paraffin-embedded placental tissues from 12 control placentas (from 23 to 39 wk) and 23 PIH placentas (from 24 to 41 wk). Reverse transcriptase-polymerase chain reaction showed that APJ was cooperatively expressed with its ligand apelin and AT1 in controls and in late-onset PIH placentas but was significantly downregulated in early-onset PIH placentas with poor fetal growth. Quantitative reverse transcriptase-polymerase chain reaction analysis revealed upregulated APJ in late-onset PIH placentas but significantly downregulated APJ in early-onset PIH. In immunohistochemical staining, APJ was detected strongly in villous capillary endothelial cells and trophoblasts of late-onset PIH placentas. In contrast, APJ was poorly stained in endothelial cells of hypoplastic villi of early-onset PIH placentas. Collective data indicate that the apelin-APJ system is involved in fetoplacental circulation during human pregnancy. Impaired APJ expression in early-onset PIH placentas may reflect an aggravated placental condition with poor fetal growth.

Comparative analysis of miRNA expression between normal and pregnancy-induced hypertension placenta

Pregnancy-induced hypertension (PIH) may threaten both maternal and fetal lives. The molecular mechanism underlying the development of PIH has not been clarified. MicroRNAs (miRNAs) have been proved to play a critical role in post-transcriptional gene regulation. Although majority of miRNAs are ubiquitously expressed in mammals, some minority of miRNAs exhibit specific expressional patterns in an organ- or cell-type-dependent manner. In this study, the profiling of miRNAs was constructed by the large-scale, high-throughput sequencing method from the normal and PIH placentas. A total of 5,368,807 and 4,954,045 miRNAs which have matched the miRNA sequence library were identified by cloning from the normal and PIH placentas respectively and three novel miRNAs which could not match the sequence library of updated miRNAs warranted further confirmation. Comparing miRNA data between normal and PIH placenta, eight microRNAs were found significantly upregulated in human PIH placentas, the majority of them were clustered on the chromosome 19 and were assumed placenta-specific. The upregulated expression of the eight miRNAs was further identified by quantitative RT-PCR assays. In summary, a significant differentiated expression between normal miRNA libraries and PIH miRNA libraries was revealed, which suggests abnormal miRNA regulation might be involved in the pathogenesis of PIH. Simultaneously, our larger-scale sequencing results has provided a general insight on exploring the pathogenesis of PIH from an miRNA-based method.

Expression of antiangiogenic prolactin fragments in the placentas of women with pregnancy induced hypertension.

It has been reported that prolactin (PRL) is cleaved to 14 or 16 kDa fragments by cathepsin D in vitro and in vivo, and that such fragments exhibit antiangiogenic and proapoptotic properties. The aim of this study was to investigate the relationship between pregnancy induced hypertension (PIH) and the placental expression of antiangiogenic PRL fragments and cathepsin D. Placental expression of PRL fragments and cathepsin D was evaluated by Western blot analysis in a group of 9 pregnant women consisting of 5 normal pregnancies and 4 severe PIH cases. Antiangiogenic PRL fragments were detected in 4 placental samples from all PIH cases but not detected in those from normal pregnancies (p<0.05). The expression of cathepsin D in PIH placentas was significantly lower than that in those without PIH (p<0.05), while the placental expression of procathepsin D was significantly greater in PIH cases than in the normal pregnancies (p<0.05). These data suggest that antiangiogenic PRL fragments in the placenta may be present only in PIH cases, and that PRL fragments in the placenta might be implicated in the pathophysiology of PIH.

Distribution of Notch family proteins in intrauterine growth restriction and hypertension complicated human term placentas

Members of the Notch family have been detected in many developmental and cell specification processes during placental development. However, Notch protein expression in Intrauterine Growth Restriction (IUGR) and Pregnancy Induced Hypertension (PIH) is not clear. In this study we aimed to clarify the immunolocalization of Notch proteins in full-term placentas after IUGR and PIH in comparison with normal placentas. Formalin-fixed, paraffin-embedded term placentas obtained by caesarean operations were processed for immunohistochemical localization of Notch 1, 2, 4 and Jagged 2. Transmission electron microscopy was also performed. In normal term placentas, all Notch proteins were intensely immunostained in the brush border of cells of the syncytiotrophoblast layer of the basal (maternal) side and the chorionic plate (fetal) side. The endothelial cells were also intensely immunostained in both sides for Notch 1. However, in IUGR and PIH placentas, the immunoreactivities of all Notch proteins were decreased significantly in the brush border of cells of the syncytiotrophoblast layer and the reaction was generally observed in the cytoplasm of syncytiotrophoblast cells in the basal and chorionic plate sides. The reactivity in endothelial cells was also significantly decreased. Our results have shown that the immunoreactivity and localization of Notch proteins is altered in pathologic placentas. Therefore, we propose that deregulated expression of Notch proteins may contribute to the disruption of trophoblast differentiation, endothelial cell function and/or feto-maternal traffic down-regulation during pregnancy or vice versa in such pathologic conditions.

Examination of the Expression of Cyclooxygenase-2 in Placenta Villi from Sufferers of Pregnancy Induced Hypertension

The purpose of this paper is to elucidate the roles of phospholipase A(2) (PLA(2)), cyclooxygenase-2 (COX-2), and prostaglandin I(2) (PGI(2)) synthase in pregnancy induced hypertension (PIH). In placentas from normal pregnant women and pregnant women with severe PIH, the enzyme expression of PLA(2), COX-2, and PGI(2) synthase was measured using real time reverse transcription-polymerase chain reaction (RT-PCR). The expression of each enzyme was compared between normal (n=12) and PIH (n=12) groups. The expression levels of COX-2 and PGI(2) synthase during PIH pregnancy were significantly decreased to about 51% and 68%, respectively, of their values in normal pregnancy. However, the expression of PLA(2) was hardly changed by PIH. The decreases in COX-2 and PGI(2) synthase expression in severe PIH placentas may be causal factors in the disruption of the PGI(2)-thromboxane A(2) (TXA(2)) balance in favor of TXA(2). The decrease in COX-2 was more marked than that of PGI(2) synthase.

Cellular Localization of Placenta-Specific Human Endogenous Retrovirus (HERV) Transcripts and their Possible Implication in Pregnancy-Induced Hypertension

We previously investigated tissue specificity and temporal changes in expression of five human endogenous retroviruses (HERVs), including syncytin/ERVWE1 and syncytin 2. In the current study, we examined the cellular localization and quantified the transcripts of five HERVs, syncytin, syncytin 2, HERV-H7/F(XA34), HERV-Fb1, and HERV-HML6-c14, in order to elucidate their physiological and etiological roles in the placenta and in pregnancy-induced hypertension (PIH), respectively. In situ hybridization revealed trophoblast-specific transcription of all five HERVs. Consistent with a previous immunohistochemical analysis, syncytin 2 transcripts were detected only in cytotrophoblasts. All the HERVs except HERV-HML6-c14 (HML6-c14) were predominantly localized in the cytoplasm of syncytiotrophoblasts and/or cytotrophoblasts. Quantitative analysis showed that transcriptional levels of these four HERVs were lower in placentas obtained from pregnant women with PIH ( n = 22) than in those from normotensive pregnant women ( n = 87) and that the differences were statistically significant ( p = 0.001, 0.01, <0.001, and 0.04 for syncytin, syncytin 2, HERV-H7/F(XA34), and HERV-Fb1, respectively). In contrast to the other HERVs, HML6-c14 transcripts localized to the nucleus and the average transcriptional level of HML6-c14 was higher in PIH placentas than in control placentas from normotensive pregnant women, although the differences did not reach significance ( p = 0.19). These results suggest that placenta-specific HERVs may have some function in the human placenta and that their reduced expression in PIH placentas is not merely a secondary effect derived from the pathology of PIH placentas.

Study on the expression of angiotensin II (ANG II) receptor subtype 1 (AT 1R) in the placenta of pregnancy-induced hypertension

Objective To study the expression of angiotensin II (ANG II) receptor subtype 1 (AT 1R) in the human placenta with pregnancy-induced hypertension (PIH). Methods Immunohistochemistry was used to detect the expression of AT 1R in placental tissues of 30 patients with PIH and 10 patients with normal pregnancies (control group). The PIH tissues were further divided into 3 groups: mild PIH group, moderate PIH group and severe PIH group. Each group consisted of 10 patients. A high-resolution pathological image analysis system (HPIAS-1000) was used to determine the quantity of AT 1R expression. Results The integral optical density and area of staining in the syncytiotrophoblast (STB) layer and villous endothelium of the placenta were significantly increased in PIH patients, in the moderate and severe PIH groups, as compared with the control group ( P<0.05), indicating that the expression of AT 1R was highly increased in PIH. However, there was no significant difference between normal pregnancy and the mild PIH group ( P>0.05). Furthermore, statistically significant differences in AT 1R expression were observed between mild, moderate and severe PIH groups ( P<0.05). Conclusion The expression of AT 1R is statistically significantly increased in the STB layer and villous endothelium of human placenta with PIH. Expression increases with the severity of the disease. Increased expression may be involved in the pathogenesis of PIH.

The expression of PLF in placenta in pregnancy-induced hypertension and the relationship between the PLF and serum VCAM-1.

To study the expression of placental isoferritin (PLF) in placental tissue of pregnancy-induced hypertension (PIH) and the relationship between the level of expression of PLF and the amount of vascular cell adhesion molecule-1 (VCAM-1) in serum, immunohistochemical technique was used to detect the expression of PLF in placenta tissue in 45 PIH patients (PIH group) and 15 normal pregnant women (normal group). High resolution pathological image analysis system (HPIAS-100) was employed to determine the quantity of PLF. The VCAM-1 in serum was examined by enzyme linked immunoabsorbent assay (ELISA). The results showed that the levels of PLF expressions in moderate and severe PIH patients were significantly lower than that of normal group (P < 0.01). The serum VCAM-1 was significantly decreased in PIH group (1310 +/- 177 rho/ng/ml) than that of normal group (609 +/- 72 rho/ng/ml, P < 0.01). The significant negative correlation existed between the expression of PLF in placental tissue and the serum VACM-1 (r = -0.58, P < 0.01). It was concluded that the level of PLF expression in PIH decreases and is negatively correlated with the amount of serum VCAM-1, indicating that these may be involved in the pathogenesis of PIH.

The immunosuppressive cytokines influence the fetal survival in patients with pregnancy-induced hypertension.

The present study examines the hypothesis that the elevated levels of transforming growth factor (TGF)-beta1 and interleukin (IL)-10 would be protective for the fetus survival during pregnancy-induced hypertension (PIH). Moreover, we evaluate the IL-12 and IL-15 serum concentrations and their relationships with PIH. Serum samples were obtained before the onset of labor from control and PIH groups. Cytokine concentrations were determined by Enzyme-Linked Immunoadsorbent Assay. Our data show that PIH women have significantly higher TGF-beta1 and IL-10 concentrations with respect to control groups (P = 0.0001). Similarly, macrophages from the PIH placentas produce in vitro more elevated TGF-beta1 and IL-10 levels compared to normal pregnant ones (P = 0.02), also in the absence of LPS stimulation. IL-12 and IL-15 serum concentrations were not detectable in all pregnant groups. We have found that PIH women have elevated concentrations of anti-inflammatory/immunosuppressive cytokines, suggesting their important role in fetal allograft protection during the normal and pathological pregnancy.

Apoptotic change in placenta of pregnancy-induced hypertension

Extravillous trophoblast cells of human placenta produce matrix-type fibrinoid, an oncofetally modified extracellular matrix. Matrix-type fibrinoid is linked to differentiation of extravillous trophoblast cells. It is involved in anchoring of the placenta to the uterine wall, at the same time enabling the trophoblast cells to migrate and to invade maternal tissues. Biochemical isolation of matrix-type fibrinoid is impossible. In vitro production is hampered by the lack of proliferation of differentiated extravillous trophoblast cells. Therefore, we want to immortalize the capability for production of matrix-type fibrinoid. In order to avoid any introduction of non human regulative genes into the trophoblastic genome, we have chosen the hybridoma technique for immortalization. Negatively selectable choriocarcinoma cell lines are available as trophoblast-related malignant parent line for fusion. Here we describe a rapid isolation protocol for differentiated term extravillous trophoblast cells. With chorion laeve as source we avoid any accidental admixture of trophoblast cells of villous origin. Immunomagnetic isolation of extravillous trophoblast cells was performed using placental alkaline phosphatase as highly trophoblast specific positive marker molecule. The relatively simple method yields preparations of differentiated extravillous trophoblast cells of high purity, which are used as second parental cell population for generation of hybridomas.

Aromatase and estrogen 2-hydroxylase activities of human placental microsomes in pregnancy-induced hypertension.

2-Hydroxylation is one of the major metabolic pathways of estrogens and is believed to be catalyzed by a form of cytochrome P450. Recently it has been reported that estrogen 2-hydroxylase activity in human placenta is catalyzed by aromatase. Some investigators suggested the effect of catechol estrogen on human placental steroidogenesis which may be related to pregnancy-induced hypertension (PIH) through the inhibition of catechol-O-methyltransferase (COMT) activity. In order to better understand the interrelationship between placental aromatase and estrogen 2-hydroxylase activities in PIH patients, both activities were evaluated in the PIH placentas. Human placental microsomes obtained from PIH patients were incubated with [1 beta-3H]androstenedione or [2-3H]estradiol in the presence of NADPH. Aromatase and estrogen 2-hydroxylase activities were assessed by the tritium water method. The immunosuppression patterns of both activities due to monoclonal antiaromatase cytochrome P450 antibody (MAb3-2C2) were studied. Estrogen 2-hydroxylase activity was significantly higher in PIH placentas (4.7 +/- 0.9 pmol/min/mg protein, n = 7) than in normal placentas (3.0 +/- 0.7 pmol/min/mg protein, n = 7). When the PIH placental microsomes were subjected to immunosuppression by 1 to 100 micrograms IgG of MAb3-2C2, estrogen 2-hydroxylase activity was suppressed by 94 to 65% whereas aromatase activity was strongly suppressed by 72 to 17%, respectively. From our results of high estrogen 2-hydroxylase activity in PIH placentas, it is assumed that there is a different estrogen catalyzing mechanism in PIH placentas.