Placenta Of Pregnant Women Research Articles

Cadmium and Lead in Women Who Miscarried.

Cadmium (Cd) and lead (Pb) are toxic elements which, when ingested excessively in food and drinking water, accumulate in selected organs and pass through the placenta barrier to the foetus, showing teratogenic effects. The aim of the study was to determine the concentration of Cd and Pb in blood and placental tissue in women who miscarried. The study group consisted of 83 women who miscarried. The control group included 35 women in the first trimester of pregnancy and after childbirth. The experimental materials consisted of whole blood and fragments of placental tissue. The concentrations of Cd and Pb were determined using atomic absorption spectrometry (AAS) with electrothermal atomization in a graphite furnace and by Inductively Coupled Plasma Mass Spectrometry (ICP-MS) in standard mode. The average concentration of Cd (2.730 ± 2.07 µg/L) and Pb (35.54 ± 11.0 µg/L) in the blood of women with miscarriage was higher in comparison to the level of these toxic metals in the blood of women from the control group (Cd 1.035 ± 0.59 µg/L; Pb 27.11 ± 4.6 µg/L). The average Cd (214.4 ± 514 µg/L) and Pb (199.6 ± 348 µg/L) content in the placenta of women with miscarriage was higher in comparison to the amount of these elements in the placenta of women from the control group (Cd 127.4 ± 85 ng/L; Pb 26.35 ± 7.9 ng/L). Tobacco smoking significantly affected cadmium blood levels and the placental tissue content in women who miscarried. Elevated Cd and Pb concentrations in the blood and placenta of pregnant women may be connected with the occurrence of miscarriage; therefore, the levels of these heavy metals should be monitored in women who plan pregnancy. It seems that determining the level of molar ratio between toxic metal and antioxidant elements can be analyzed as a marker for selection for control examinations as a valuable complement to existing diagnostic procedures in prevention, especially in early pregnancy. Additional diagnostic methods should be established as new tools in perinatal care in order to enable early diagnosis of pregnancy pathology and, especially, to prevent miscarriage.

Parity improves anti-tumor immunity in breast cancer patients.

Compared to nulliparous women, parous women have an up to 50% lower lifetime risk of developing breast cancer. An endogenous mechanism to prevent the development of cancer is the destruction of tumor cells by T cells that recognize tumor-associated antigens (TAA). Since a number of TAA are also highly present in the breast and placenta of pregnant women, we investigated the induction and characteristics of spontaneous T cell responses against TAA during pregnancy.To this end, we collected peripheral blood from healthy nulliparous, primigravid and parous women, as well as from breast cancer patients. IFN-γ ELISpot assays were performed to measure the intensity and specificity of T cell responses against 11 different TAA. The impact of TAA-specific Treg cells on anti-TAA responses was assessed by performing the assay before and after depletion of CD4+CD25+ T cells. The antigenic specificities of these Treg cells were analyzed by the Treg specificity assay. Furthermore, we conducted flow cytometric analyses to determine the memory phenotype and cytokine secretion profile of TAA-specific T cells.Our results demonstrate that pregnancy induces functional and long-lived memory and effector T cells that react against multiple TAA. These persist for many decades in parous females, but are not found in age-matched females without children. We also detected TAA-specific Treg cells, which suppressed strong effector T cell responses after delivery. Nulliparous breast cancer patients displayed median TAA-specific effector T cell responses to be decreased threefold compared to parous patients, which could be restored in vitro after depletion of Treg cells.

Improvement of a tissue maceration technique for the determination of placental involvement in schistosomiasis.

Schistosomiasis in pregnancy may cause low birth weight, prematurity and stillbirth of the offspring. The placenta of pregnant women might be involved when schistosome ova are trapped in placental tissue. Standard histopathological methods only allow the examination of a limited amount of placental tissue and are therefore not sufficiently sensitive. Thus, placental schistosomiasis remains underdiagnosed and its role in contributing to schistosomiasis-associated pregnancy outcomes remains unclear. Here we investigated an advanced maceration method in order to recover a maximum number of schistosome ova from the placenta. We examined the effect of different potassium hydroxide (KOH) concentrations and different tissue fixatives with respect to maceration success and egg morphology. Placental tissue was kept either in 0.9% saline, 5% formalin or 70% ethanol and was macerated together with Schistosoma mansoni infested mouse livers and KOH 4% or 10%, respectively. We found that placenta maceration using 4% KOH at 37°C for 24 h was the most effective method: placental tissue was completely digested, egg morphology was well preserved and alkaline concentration was the lowest. Ethanol proved to be the best fixative for this method. Here we propose an improved maceration technique in terms of sensitivity, safety and required skills, which may enable its wider use also in endemic areas. This technique may contribute to clarifying the role of placental involvement in pregnant women with schistosomiasis.

Expression of apelin in serum and placenta of pregnant women with severe preeclampsia

目的 研究重度子痫前期患者外周血清、脐血清、胎盘组织中apelin水平及其受体APJ（apelin receptor）在胎盘组织中的表达水平，以及apelin与胎盘重量和新生儿出生体重的关系，探讨apelin在子痫前期发病中的作用。 方法 选取2014年5月至12月在我院住院分娩的单胎、重度子痫前期孕妇28例为子痫前期组，同期正常孕妇20例为对照组。采用酶联免疫吸附试验法检测孕妇外周血清及脐血清中apelin水平，免疫组织化学法检测胎盘组织中apelin及APJ的表达情况。采用t检验，以及Pearson相关分析进行统计学分析。 结果 （1）与对照组相比，子痫前期组的母体外周血清及脐血清中apelin水平较高[分别为（46.27±7.40）与（70.08±11.35） pg/ml、（59.55±3.44）与（71.20±7.90） pg/ml，t值分别为8.210和6.180]，但新生儿出生体重及胎盘重量较低[分别为（3 290.0±443.0）与（1 958.9±466.1） g、（551.2±78.3）与（321.9±98.1） g，t值分别为－9.960和－8.660]（P值均<0.05）。（2）子痫前期组中apelin和APJ蛋白在胎盘组织滋养层细胞质中均低表达，其平均光密度值均低于对照组（分别为0.20±0.03与0.28±0.04、0.22±0.04与0.29±0.07，t值分别为-6.647和3.665，P值均<0.05）。（3）子痫前期组中，外周血清apelin水平与新生儿出生体重及胎盘重量呈负相关（r值分别为－0.662和－0.469），脐血清apelin水平与新生儿出生体重及胎盘重量呈负相关（r值分别为－0.560和－0.400），胎盘组织apelin水平与新生儿出生体重及胎盘重量呈正相关（r值分别为0.447和0.293）（P值均<0.05）。 结论 子痫前期患者外周血清、胎盘组织、脐带血清中apelin水平发生显著变化，提示apelin参与了子痫前期的发病。

Placental Morphology of Pregnant Iraqi Women with Rheumatic Heart Disease

Background: Placental morphology and cellular arrangement can be altered in maternal diseases. Rheumatic heart disease (RHD) is a chronic heart condition that can lead to death in pregnant women. The aim of this study is to determine the histological changes of the placenta in pregnant women suffering from RHD. Methods: Placentae were collected from 10 healthy pregnant women, and 31 pregnant women with heart conditions (26 with RHD and 5 with NRHD) who had been admitted to the Baghdad Teaching Hospital. Placental tissues were fixed in 10% formal-saline and were processed for light microscopy. Measurements including the placental weight and diameter of the chorionic villi capillaries were recorded. Results: The results indicate that there are many histological changes in pregnant women with RHD such as hyalinisation, fibrosis of the chorionic villi, proliferation of trophoblastic cells, and thickening of its membrane. Additionally, expectant mothers with RHD experience a reduction in capillary diameter and thickening of the capillary walls, and decreased size and weight of their placenta when compared with the control. Conclusions: Heart diseases, especially RHD, are associated with developmental damage of the placenta in pregnant women by injuring the endothelial cells of the placentas capillaries.

Затримка росту плода: діагностика та перинатальні наслідки

The objective: to determine the importance of a comprehensive ultrasound check of a foetus with arrested development. Patients and methods. Some 185 pregnant women with foetuses with arrested development were examined, including their amniotic fluid volume and Doppler velocimetry of foetal circulation. Results. Reliable changes in the placenta, amniotic fluid volume and Doppler parameters of fetal circulation. Conclusions. The stages and scale of the pathological process in a foetus with arrested development can be clearly determined with the help of a comprehensive ultrasound check. Key words: intrauterine growth restriction, pregnancy, blood flow in the uterus and placenta of pregnant women and in foetuses, Doppler.

Morphological changes in the placenta of pregnant women with gestation period more than 40 weeks

The article presents some data of a morphological research of the placenta in pregnant women with period of gestation more than 40 weeks.We examined 30 placentas in this group of pregnant women, and different disorders and changes in the microcirculation. As a result of disorders in the microcirculation there are morphological and functional compensatory changes in the placenta first, which manifest themselves with additional growth of terminal cilia and small capillaries. Further changes are characterized by the development of subcompensated and decompensated changes, which are characterized by extension of capillaries in the terminal cilia and growth of the perivascular edema. Progression of disorders leads to formation of vessel-free zones, possibility of heart attacks.

Abnormal expression of inflammatory genes in placentas of women with sickle cell anemia and sickle hemoglobin C disease.

Sickle cell disease (SCD) is a complex disease that is characterized by the polymerization of deoxyhemoglobin S, altered red blood cell membrane biology, endothelial activation, hemolysis, a procoagulant state, acute and chronic inflammation, and vaso-occlusion. Among the physiological changes that occur during pregnancy, oxygen is consumed by fetal growth, and pregnant women with SCD are more frequently exposed to low oxygen levels. This might lead to red blood cells sickling, and, consequently, to vaso-occlusion. The mechanisms by which SCD affects placental physiology are largely unknown, and chronic inflammation might be involved in this process. This study aimed to evaluate the gene expression profile of inflammatory response mediators in the placentas of pregnant women with sickle cell cell anemia (HbSS) and hemoglobinopathy SC (HbSC). Our results show differences in a number of these genes. For the HbSS group, when compared to the control group, the following genes showed differential expression: IL1RAP (2.76-fold), BCL6 (4.49-fold), CXCL10 (-2.12-fold), CXCR1 (-3.66-fold), and C3 (-2.0-fold). On the other hand, the HbSC group presented differential expressions of the following genes, when compared to the control group: IL1RAP (4.33-fold), CXCL1 (3.05-fold), BCL6 (4.13-fold), CXCL10 (-3.32-fold), C3 (-2.0-fold), and TLR3 (2.38-fold). Taken together, these data strongly suggest a differential expression of several inflammatory genes in both SCD (HbSS and HbSC), indicating that the placenta might become an environment with hypoxia, and increased inflammation, which could lead to improper placental development.

Морфологічні особливості плаценти при прееклампсії за даними гістохімії

One of the important stages in analyzing the causes of complications of pregnancy and childbirth, particularly preeclampsia, is considered to be a natural morphological study of the placenta. The main direction of research is to identify morphological of diagnostic and prognostic criteria of preeclampsia in general, and special lesions of structures of the placenta in particular. The objective: to study the morphological features of the placenta in pregnancy complicated by preeclampsia varying severity according histochemistry and prediction of the potential cardiovascular risks in the future. Patients and methods. Histochemical study of the placenta of women whose pregnancy was complicated by preeclampsia (PE). The first group consisted of placentas from 12 women with mild PE; group II - 9 placentas from women with moderate and severe PE; III group (control) consisted of 15 placentas from women without obstetric and somatic pathology and signs of PE. Comprehensive evaluation of structural features of the placenta included macroscopic examination, organometry and review histology. Results. In the placenta of pregnant women mainly with moderate and severe PE detected in the decidua basalis of individual macrophages with pronounced soudaniennes cytoplasm; thrombosis in the majorsince space, discirculatory disorders in form of ischemic infarcts and compensatory-adaptive reactions according to the type of angiomatosis of individual villis; in the vessels of the placenta and decidual shell identified phenomen of atherosis of the different degree of severity. Conclusion. In women with PE in placenta revealed disorders of lipid metabolism,which may indicate its involvement in the pathogenesis of this disease continue to be one of the prognostic criteria of risk of the development of atherosclerosis and one of the first signals to metabolic disturbances. Key words: preeclampsia, placenta, histochemistry, thrombosis, atherosis, angiomatosis.

Expression of Hepcidin and Ferroportin in the Placenta, and Ferritin and Transferrin Receptor 1 Levels in Maternal and Umbilical Cord Blood in Pregnant Women with and without Gestational Diabetes.

Background: Regulation of iron transfer from mother to fetus via the placenta is not fully understood and the relationship between stored iron status in the mothers’ serum and gestational diabetes (GDM) in case–control studies is controversial. The present study aimed to detect circulating soluble transferrin receptor (sTfR) and ferritin levels in maternal and umbilical cord blood. We also examined the expression of hepcidin (Hep), transferrin receptor (TfR1), and ferroportin (FPN) in the placenta in pregnant women with and without GDM at full term. Methods: Eighty-two women participated (42 with GDM and 40 without GDM [controls]). Maternal samples were collected at 37–39 weeks’ gestation. Umbilical cord blood was collected at birth. Ferritin and sTfR levels in maternal serum and umbilical cord blood, and Hep, TfR1, and FPN protein expression in plac enta were compared between the GDM and non-GDM groups. Serum ferritin (SF) was measured by electrochemiluminescence assay and sTfR was measured by ELISA. Hep, TfR1, and FPN expression was measured by immunohistochemistry. Results: Maternal serum sTfR levels were significantly elevated in the GDM group compared with the non-GDM group (p = 0.003). SF levels in cord blood in the GDM group were significantly higher than those in the non-GDM group (p = 0.003). However, maternal hemoglobin and SF, and umbilical cord sTfR levels were not different between the groups. In placental tissue, FPN expression was higher and hepcidin expression was lower in the GDM group compared with the non-GDM group (p = 0.000 and p = 0.044, respectively). There was no significant difference in TfR1 between the groups (p = 0.898). Conclusions: Women with GDM transport iron more actively than those without GDM at term pregnancy. Maternal iron metabolism in GDM may play a role in fetal/placental iron demand and in the overall outcome of pregnancy.

12 Expression of corticotropin-releasing hormone in the placentas of pregnant women with hypertensive disorders

Introduction the human placenta is an extrahypothalamic site for the synthesis and secretion of corticotropin-releasing hormone (CRH). Receptors CRH-R1 and CRH-R2 are expressed in the syncytiotrophoblast, in the cytotrophoblast, in the decidua, and in the vascular endothelium. Studies have showed an increased expression of CRH in cases with preeclampsia. Objective this study aimed to evaluate the expression of CRH in the chorionic villi and in the decidua of human placentas of women with different types of hypertensive disorders of pregnancy (HDP). Methods 116 placental biopsies collected from 2013 to 2014 were analyzed, and they were grouped as follows: (a) control group (C): 12 cases; (b) gestational hypertension (GH): 23 cases; (c) preeclampsia/eclampsia (PE): 30 cases; (d) chronic hypertension (CH) 25 cases and (e) preeclampsia superimposed on chronic hypertension (PSCH): 26 cases. Of these cases, 54 biopsy samples were from preterm deliveries ( ⩾ 37 weeks). The expression of CRH in the chorionic villi and in the decidua was assessed by immunohistochemistry; the immunostained areas were quantified using Leica Qwin Plus® image analysis software and expressed as percentage of positive area per field. ANOVA (F) followed by Tukey’s test was used for statistical analysis; p 0.05. Results 33.33% (18) of preterm pregnancies were diagnosed with PE, 20.37% (11) were diagnosed with GH, 20.37% (11) had CH, and 25.93% (14) had PSCH; whereas 19.35% (12) of term pregnancies had PE, 19.35% (12) were diagnosed with GH, 22.58% (14) had CH, 19.35% (12) PSCH, and 19.35% (12) were control cases. In term pregnancies, cases with PE, GH, CH and PSCH showed an increased expression of CRH in the chorionic villi and in the decidua than group C (p 0.0001). In the preterm group, the expression was higher in cases associated with PE and PSCH in both regions. Conclusions altered expression of CRH is observed in HDP, and it occurred in all types of term HDP in both regions analyzed. In preterm pregnancies, expression was more prominently increased in the decidua of the PE and PSCH cases. Therefore, CRH expression behaved similarly in term pregnancy cases with HDP, but the expression varied in the preterm cases associated with PE, thus demonstrating that the levels of placental oxidative stress were higher in these cases. Download : Download high-res image (372KB) Download : Download full-size image

26 Inflammasome activation in placenta from pregnant women with preeclampsia

Introduction Preeclampsia (PE) is a pregnancy disorder characterized by an imbalance between pro- and anti-inflammatory cytokines associated with high plasma levels of uric acid and Interleukin-1 beta (IL-1 β ) in the severe cases of PE. Uric acid acts as a danger-associated molecular pattern (DAMP) and activates the inflammasome in the trophoblast cells, leading to IL-1 β secretion. Inflammasomes are intracellular multiprotein complexes which mediate innate immune response via caspase-1 activation, resulting in IL-1 β and IL-18 secretion in their active forms. Objectives As placenta seems to play an important role in the pathogenesis of PE the present study aimed to investigate the expression of gene and proteins related to the inflammasome in placenta from preeclamptic women. Methods Placental tissue was collected from 20 normotensive pregnant women and 20 preeclamptic women, and NLRP3, caspase-1, IL-1 β , tumor necrosis factor-alpha (TNF- α ) , IL-18 and high-mobility group box 1 protein (HMGB1) were evaluated by immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), and also analyzed by quantitative real-time polymerase chain reaction (RT-qPCR). Results Placenta from pregnant women with PE showed increased mRNA expression for NLRP3, caspase-1, IL-1 β and TNF- α as well as their protein expression. Higher levels of caspase 1, IL-1 β and TNF- α were detected by ELISA in placental homogenate of preeclamptic group than in normotensive group. Lower expression of mRNA for IL-18 and its protein expression were detected in placenta of pregnant women with PE compared with normotensive group. No significant differences were observed between control and preeclamptic groups in relation to HMGB1 gene and protein expression. Conclusion The results suggest that placenta from pregnant women with preeclampsia shows activation of NLRP3 inflammasome which may be involved in the exaggerated inflammatory state detected in women with preeclampsia. Financial support: Fapesp 2012/24697-8 and 2013/00535-1

Effects of passive smoking on terminal villi of human placenta and growing foetus

Background : Though ill effects of maternal smoking on growing foetus and placenta is well established, passive/ second hand smoking has recently been implicated as another potential risk factor. The incidence of low birth weight, Intra-Uterine Growth Retardation (IUGR), prematurity and stillbirth has been associated with passive smoking. Our study focuses on the gross and histological changes in the full term placenta of women exposed to passive smoke from a close member of a family smoking at least 20 cigarettes/bidis per day. Method: The present study is an endeavour to observe microscopic features (light microscope under 10X and 40X only) of placenta of pregnant women who are exposed to environmental tobacco smoke from a close member of the family and simultaneously observe changes on growing foetus during level II ultrasound at 2 nd trimester in terms of IUGR if any. This is a descriptive study with statistical analysis done using ‘Independent Sample Test’. Results : The histopathological changes seen in the placenta of passive smokers were almost alike to active smokers showing increased syncytial knots, hyperplasia of cytotrophoblast cells and proliferation of fetal capillaries. However no significant IUGR was noticed during Level II USG of the fetuses. Conclusion : On gross findings there was a definite co-relation with low birth weight babies born to passive smokers and a compensatory enlargement of the placenta. The microscopic changes seen in the placenta of passive smokers was a consistent finding similar to ischemic changes. No definite relationship could be established between the histological changes observed amongst passive smokers and IUGR seen in the growing foetus .

Inducible nitric oxide synthase in the placenta of pregnant women with preeclampsia

Preeclampsia (PEC) is the cause of fetal and maternal death. Inducible nitric oxide synthase (iNOS) found in macrophages, smooth muscle cells and endothelial cells. The main objective was to detect the fluorescence iNOS in placenta. Cotyledons cuts were made, they were placed in 10% formalin. And on the slides washed with buffer solution, oxygenated water with methanol, using 10% pig serum, anti iNOS Rabbit pAb solution, streptavidin-fluorescein. Microscope Carl Zeiss and Image-Pro 7.0 software was used. Placentas of pregnant women with PEC without pathology were analyzed. Increased uptake of fluorescein in erythrocytes of women without PEC was found, patients who developed PEC was remarkable decreased uptake of fluorescein. Decreasing iNOS activity is evident in preeclampsia.

62-OR

Objectives Autophagy is a lysosomal degradation pathway that removes protein aggregates and damaged organelles maintaining the cellular integrity. It is an inducible process that responds to the environment and it seems to be essential for cell survival during stress, starvation, hypoxia and consequently to the placenta implantation and development. Studies on the role of autophagy in placenta from pregnant women with preeclampsia are scarce and still unclear. The aim of this study was to compare the expression of autophagy-related proteins, LC3-II, beclin-1 as well as mTOR protein in placental tissue from pregnant women with preeclampsia and normotensive pregnant women. Methods The expression of LC3-II and beclin-1 proteins involved in the autophagosome formation as well as mTOR protein was evaluated in 18 placentas of pregnant women with preeclampsia and in 20 of normotensive pregnant women who had elective cesarean delivery before the onset of labor. Fragments of the placenta were obtained immediately after delivery and the samples were prepared for real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemistry and transmission electron microscopy analysis. Results LC3-II expression as detected by RT-qPCR was significant higher in placentas of normotensive pregnant women compared with preeclamptic women. No significant difference in beclin-1 and mTOR expression was seen between these two groups. LC3-II, beclin-1 and mTOR proteins were detected by immunohistochemistry in syncytiotrophoblast and cytotrophoblast in both groups, and the presence of autophagic vacuoles containing intracytoplasmatic organelles was confirmed with electron microscopy. Conclusions The results of the impaired autophagy demonstrated by decrease of LC3- II expression in placenta of preeclamptic patients might play a role in the pathophysiology of preeclampsia. Financial support: FAPESP 2013/00535-1 and 2012/24697-8. Disclosures I.C. Weel: None. V.R. Ribeiro: None. M. Romao: None. M.L. Matias: None. V.T. Borges: None. J.C. Peracoli: None. J.P. Araujo Jr: None. M.T. Peracoli: None.

Морфологическая характеристика плаценты у беременных женщин с сифилитической инфекцией

Морфологическая характеристика плаценты у беременных женщин с сифилитической инфекцией

Hyperexpression of Inflammatory Genes in Placental Tissue in Patients with Hemoglobin SC Disease

Introduction: Pregnant women with sickle cell disease (SCD) are at higher risk of obstetrical complications, such as preeclampsia and preterm delivery. The placental circulation is susceptible to vaso-occlusion, which may contribute to fibrosis, necrosis and infarction of the placental villi. Restricted uteroplacental circulation is associated with low birth weight and fetal growth restriction. The mechanisms by which SCD affects placental physiology are largely unknown, and the chronic inflammatory state may be involved in this pathological process. The aim of this study was to evaluate the expression of mediators of inflammatory response in the placenta of pregnant women with SCD.Methods: This is an ongoing case control study that has recruited 4 pregnant patients with hemoglobin SC disease and 4 healthy control pregnant women paired for gestational age and route of delivery. Placental tissue was collected for total RNA extraction and synthesis of cDNA. Samples were run on a qPCR Array (Inflammatory Response and Autoimmunity RT2 Profiler, Qiagen), which includes 84 genes. Gene expression levels were normalized to housekeeping genes (ACTB, B2M, and RPLP0), and will be further validated by RT-qPCR.Results: Two patients underwent cesarean delivery and one patient delivered preterm. The analysis of placental gene expression showed that 16 genes were upregulated. The top 5 most upregulated genes were CCL24 (18.1 fold), TLR9 (8.6 fold), inducible nitric oxide synthase NOS2 (6.8 fold), IL17A (5.4 fold), and CCL16 (4.8 fold). Upregulated genes also included other chemokines and their receptors (CCL21, CCL22, CXCL3, and CCR7), interleukins (IL1RAP, IL5, and IL9), another toll-like receptor (TLR3), transcription factor BCL6, CD40 ligand (CD40LG), and kininogen 1 (KNG1). Interestingly, the two genes found to be downregulated were CRP (C reactive protein) and IFNG (interferon gamma).Conclusion: This is the first study of differential gene expression in placenta of patients with SCD. Despite patients with hemoglobin SC disease being clinically less severe than homozygous sickle cell anemia, we have found that placental tissue in this subset of patients displays increased expression of several genes involved in inflammatory response. Our data support local inflammatory changes in the placenta of these patients that might explain the development of complications in SCD pregnancies. Although the association between obstetric complications and SCD has been long described, our data should contribute to better define the mechanisms affecting the placental physiology that lead to complications, such as preeclampsia. DisclosuresNo relevant conflicts of interest to declare.

Myostatin in the placentae of pregnancies complicated with gestational diabetes mellitus

IntroductionGestational diabetes mellitus (GDM) is characterised by maternal glucose intolerance and insulin resistance during pregnancy. Myostatin, initially identified as a negative regulator of muscle development may also function in the regulation of placental development and glucose uptake. Myostatin expression in placentae of GDM complicated pregnancies is unknown. However, higher myostatin levels occur in placentae of pregnancies complicated with preeclampsia. We hypothesise that myostatin will be differentially expressed in GDM complicated pregnancies. MethodsMyostatin concentrations (ELISA) were evaluated in plasma of presymptomatic women who later developed GDM and compared to plasma of normal glucose tolerant (NGT) women. Furthermore, myostatin protein expression (Western blot) was studied in placentae of pregnant women with GDM (treated with diet or insulin) compared to placentae of NGT women. ResultsNo significant difference in myostatin concentration was seen in plasma of pre-symptomatic GDM women compared to NGT women. In placenta significant differences in myostatin protein expressions (higher precursor; p < 0.05and lower dimer: p < 0.005) were observed in GDM complicated compared to NGT pregnancies. Furthermore, placentae of GDM women treated with insulin compared to diet have higher dimer (p < 0.005) and lower precursor (p < 0.05). Compared to lean women, placentae of obese NGT women were lower in myostatin dimer expression (p < 0.05). DiscussionMyostatin expression in placental tissue is altered under stress conditions (e.g. obesity and abnormal glucose metabolism) found in pregnancies complicated with GDM. We hypothesise that myostatin is active in these placentae and could affect glucose homoeostasis and/or cytokine production thereby altering the function of the placenta.

Immunohistochemical properties of the expression of endothelial nitric oxide synthase in placenta in its dysfunction in women with iron deficiency anemia

Aim. The pertinence of the study is related to a large prevalence of dysfunction of the placenta in pregnant women suffering from anemia. To evaluate the immunohistochemical expression characteristics of endothelial NO-synthase (eNOS) in the placenta during its dysfunction in women against the background of anemia 30 samples of placental tissue were studied with the use of immunohistochemical and micrometer methods.Mеthods and results. It was found that the expression of eNOS in patients with iron deficiency anemia in the cytoplasm of syncytium of villi and fetal capillary endothelium as well as decidual vessels decreases, with the most pronounced changes in the expression of eNOS observed in the presence of the combination of placental dysfunction and iron deficiency anemia in the form of paradoxical increase in expression.Conclusion. This indicates the necessity for correction of endothelial function in women with anemia during pregnancy.

Role of lectin-like oxidized low density lipoprotein-1 in fetoplacental vascular dysfunction in preeclampsia.

The bioavailability of nitric oxide (NO) represents a key marker in vascular health. A decrease in NO induces a pathological condition denominated endothelial dysfunction, syndrome observed in different pathologies, such as obesity, diabetes, kidney disease, cardiovascular disease, and preeclampsia (PE). PE is one of the major risks for maternal death and fetal loss. Recent studies suggest that the placenta of pregnant women with PE express high levels of lectin-like oxidized LDL receptor-1 (LOX-1), which induces endothelial dysfunction by increasing reactive oxygen species (ROS) and decreasing intracellular NO. Besides LOX-1 activation induces changes in migration and apoptosis of syncytiotrophoblast cells. However, the role of this receptor in placental tissue is still unknown. In this review we will describes the physiological roles of LOX-1 in normal placenta development and the potential involvement of this receptor in the pathophysiology of PE.