Pathophysiology Of Preeclampsia Research Articles

Identification of LncRNA-miRNA-mRNA ceRNA network in hypoxia-induced HTR-8/SVneo cells for preeclampsia.

Preeclampsia (PE) is a common pregnancy complication, and placental hypoxia is one of its causes. We aimed to identify the transcriptional profile and construct a long non-coding RNAs (lncRNA)-centered competing endogenous RNAs (ceRNA) network in hypoxia-induced HTR8/SVneo cells. We used datasets from the GEO database to identify important pathways in PE. We performed microarray profiling and functional analysis to identify differentially expressed long non-coding RNAs (lncRNAs), differentially expressed profiles of microRNA (miRNAs), and differentially expressed profiles of messenger RNA (mRNAs) in hypoxia-induced HTR8/SVneo cells. The candidates were validated using quantitative reverse transcription polymerase chain reaction. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses were performed to understand the functional significance of differentially expressed genes. Finally, we constructed an lncRNA-centered ceRNA network. Several hub genes were validated both in placentas from PE and normal pregnancy, and in hypoxia-induced HTR8/SVneo cells. The hypoxic response pathway was involved in the pathophysiology of PE. Subsequently, we identified 536 differentially expressed profiles of lncRNAs (183 upregulated and 353 downregulated), 46 differentially expressed profiles of miRNAs (35 upregulated and 11 downregulated), and 2782 differentially expressed profiles of mRNAs (DEmRNAs) (1031 upregulated and 1751 downregulated) in hypoxia-induced HTR8/SVneo cells. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed potential pathways affected by these genes, such as angiogenesis, the HIF-1 signaling pathway, and the PI3K-Akt signaling pathway. The ceRNA network comprised 35 lncRNAs, 11 miRNAs, 27 mRNAs, and 2 hub lncRNAs, which might play a vital role in placental functions and PE. Our results revealed the transcriptome profile and constructed an lncRNA-centered ceRNA network in hypoxia-induced HTR8/SVneo cells, thereby providing potential therapeutic targets for PE.

Vitamin D may alleviate pre-eclampsia by modulating the ferroptosis signalling pathway: A hypothesis based on recent literature.

Ferroptosis is a novel form of regulated cell death typically characterized by non-apoptotic, iron-dependent, and reactive accumulation of oxygen species. Recent studies have found that ferroptosis plays an important role in the pathophysiology of pre-eclampsia (PE). In order to find potential therapeutic targets for ferroptosis intervention and better prevent the occurrence and progression of PE, the signalling pathways that regulate ferroptosis need to be identified. In this article, we review the role of vitamin D in PE and the role of ferroptosis in PE. Based on recent literature, we propose the scientific hypothesis that vitamin D can alleviate preeclampsia by modulating the ferroptosis signalling pathway. The aim of this review is to understand the regulatory pathways of ferroptosis in PE and to identify potential therapeutic targets.

Tissue Factor Pathway Inhibitors as Potential Targets for Understanding the Pathophysiology of Preeclampsia.

Preeclampsia is a hypertensive disorder of pregnancy that causes maternal and perinatal morbidity and mortality worldwide. Preeclampsia is associated with complex abnormalities of the coagulation and fibrinolytic system. Tissue factor (TF) is involved in the hemostatic system during pregnancy, while the Tissue Factor Pathway Inhibitor (TFPI) is a major physiological inhibitor of the TF-initiated coagulation cascade. The imbalance in hemostatic mechanisms may lead to a hypercoagulable state, but prior research has not comprehensively investigated the roles of TFPI1 and TFPI2 in preeclamptic patients. In this review, we summarize our current understanding of the biological functions of TFPI1 and TFPI2 and discuss future directions in preeclampsia research. A literature search was performed from inception to 30 June 2022 in the PubMed and Google Scholar databases. TFPI1 and TFPI2 are homologues with different protease inhibitory activities in the coagulation and fibrinolysis system. TFPI1 is an essential physiological inhibitor of the TF-initiated extrinsic pathway of coagulation. On the other hand, TFPI2 inhibits plasmin-mediated fibrinolysis and exerts antifibrinolytic activity. It also inhibits plasmin-mediated inactivation of clotting factors and maintains a hypercoagulable state. Furthermore, in contrast to TFPI1, TFPI2 suppresses trophoblast cell proliferation and invasion and promotes cell apoptosis. TFPI1 and TFPI2 may play important roles in regulating the coagulation and fibrinolytic system and trophoblast invasion to establish and maintain successful pregnancies. Concentrations of TF, TFPI1, and TFPI2 in maternal blood and placental tissue are significantly altered in preeclamptic women compared to normal pregnancies. TFPI protein family may affect both the anticoagulant (i.e., TFPI1) and antifibrinolytic/procoagulant (i.e., TFPI2) systems. TFPI1 and TFPI2 may function as new predictive biomarkers for preeclampsia and navigate precision therapy.

Placental exosomal miR-125b triggered endothelial barrier injury in preeclampsia

IntroductionPreeclampsia (PE) is an elusive life-threatening complication of pregnancy, and maternal endothelial dysfunction induced by components from the impaired placenta is a key hallmark of PE. Placenta-derived exosomes in maternal circulation have been correlated with risk of PE, however, the role of exosomes in PE remains to be determined. We hypothesized that placenta-released exosomes link the placental abnormalities with maternal endothelial dysfunction in PE. MethodsCirculating exosomes were collected from plasma samples of preeclamptic patients and normal pregnancies. Endothelial barrier function was examined by transendothelial electrical resistance (TEER) and cell permeability to FITC-dextran assays in human umbilical vein endothelial cells (HUVECs). miR-125b and VE-cadherin gene expression in exosomes and endothelial cells were assessed by qPCR and Western, and the possible post-transcriptional regulation of miR-125b on VE-cadherin was detected by luciferase assay. ResultsWe isolated placenta-derived exosomes in the maternal circulation and found that placenta-derived exosomes from preeclamptic patients (PE-exo) leads to endothelial barrier dysfunction. We then identified decreased expression of VE-cadherin in endothelial cells contribute to the breakdown of the endothelial barrier. Further investigations revealed increased exosomal miR-125b in PE-exo directly inhibited VE-cadherin in HUVECs, thereby mediating the adverse effect of PE-exo on endothelial barrier function. DiscussionPlacental exosomes link impaired placentation and endothelial dysfunction, thus providing new insight into the pathophysiology of preeclampsia. Exosomal miRNAs derived from placenta contribute to the endothelial dysfunction in PE and could be a promising therapeutic target for PE.

The Distribution of Foxp3 and CD68 in Preeclamptic and Healthy Placentas: A Histomorphological Evaluation.

Preeclampsia is a complication of pregnancy that affects 3-5% of pregnancies and is one of the major causes of maternal/neonatal mortality and morbidities worldwide. We aimed to investigate the distribution of Foxp3+ regulatory T-cells and CD68+ Hofbauer cells in the placenta of preeclamptic and healthy pregnant women with a special focus on correlating these findings with placental histology. Decidua and chorionic villi of the placenta obtained from healthy and preeclamptic pregnancies were evaluated in full-thickness sections. Sections were stained with hematoxylin and eosin and Masson's trichrome and immunostained for Foxp3 and CD68 for histological analyses. The total histomorphological score for placentas was found to be higher in preeclamptic placentas than that in the controls. The CD68 immunoreactivity was higher in the chorionic villi of preeclamptic placentas than that in the controls. The immunoreactivity of Foxp3 was found widely distributed within the decidua in both the groups and did not differ significantly. Interestingly, Foxp3 immunoreactivity in the chorionic villi was found mainly in the villous core and, to a lesser extent, in the syncytiotrophoblasts. We found no significant relation between Foxp3 expressions and morphological changes observed in preeclamptic placentas. Although extensive research is being carried out regarding the pathophysiology of preeclampsia, the findings are still controversial.

Hypertensive Disorder in Pregnancy and Pre-eclampsia

Background: Frequently, hypertension (high blood pressure) or its disorder occurs during pregnancy, and it remains one of the major causes of maternal and fetal mortality and morbidity associated with pregnancy, as well as the risk of pregnant women with hypertension during pregnancy to cardiovascular disease later in life. However, contrary to the general hypertension guidelines, the reasons for this report include the benefit of normalizing treatment of high blood pressure in pregnant women and potential risks related to decreased prenatal chorionic perfusion, and exposure of the uterus to antihypertensive drugs. This approach is based on a review of previous reports and literature and includes a taxonomic review of the types of blood pressure during pregnancy, the physiological changes in pregnancy that affect blood pressure disorders, the immediate and long-term consequences of hypertension, and the pathophysiology of pre-eclampsia that are related to the disturbance of proteinuria in the body, and the goals of hypertension treatment may reduce meternal severe effects without increased risk of pregnancy loss or neonatal care at a high level. The critical need to investigate the social and economic variables that contribute to the inequities in maternal health care is discussed in our final discussion on the field's research future.
 so it is necessary to know the pressure and treat it immediately. Failure to treat high blood pressure can lead to maternal morbidity and mortality, especially during childbirth, or the loss of the fetus significantly.
 Therefore, in this mini review, we will try to discuss high blood pressure in pregnant women and determine the goals of treatment and preeclampsia caused by high blood pressure.
 The aim of the review is a quick scientific summary of this disorder that has become common at the present time.Conclusions : Medical consultation should be done in order to improve the health of the mother, as well as the use of optimal medication and pre-pregnancy management in women with or threatened with high blood pressure, and we consider it necessary to inform them of the increased risks to her health and the health of the fetus.
 Strategies must be in place to predict those most at risk and to determine optimal drug therapies to minimize adverse pregnancy outcomes

Understanding the Role of Chemerin in the Pathophysiology of Pre-Eclampsia.

Chemerin is a multifaceted adipokine that is involved in multiple biological processes, including inflammation, angiogenesis, adipogenesis, and energy metabolism, as well as oxidative stress. There is a vast body of evidence for a crucial role of chemerin in the development of different cardiovascular diseases. Blood chemerin levels, as well as its placental expression, are elevated in patients with pre-eclampsia (PE) and correlate positively with the severity of the disease. This narrative review summarizes the current knowledge about the potential role of chemerin during PE development, with a particular focus on its involvement in oxidative stress and endothelial dysfunction.

Transcriptomic profiling in hypoxia-induced trophoblast cells for preeclampsia

This study aimed to identify the expression profile of mRNAs and analyze the associated pathways in hypoxia-induced trophoblast cells to understand the effect of hypoxia on the pathophysiology of preeclampsia (PE). We downloaded two gene expression datasets (GSE47187 and GSE60432) from the Gene Expression Omnibus (GEO) datasets to identify altered transcriptomes. GEO2R, gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) networks were used to reveal the functional roles and regulatory networks of the differentially expressed genes (DEGs). In total, 224 DEGs (91 upregulated and 133 downregulated) were identified, and the “HIF-1 signaling pathway” was activated in placentas from patients with PE. We validated the expression levels of five proteins in the plasma of NP and PE patients during early or late pregnancy using western blotting. In primary trophoblast cells cultured under hypoxic conditions, 754 DEGs were identified, including 362 upregulated and 392 downregulated genes. These DEGs were associated with the “HIF-1signaling pathway,” “response to hypoxia,” and several glucose metabolism pathways. In addition, a PPI network was constructed, and an important module, including 18 hub genes, was identified. Finally, we validated 18 hub genes using qRT-PCR. Furthermore, we performed microarray profiling of hypoxia-treated HTR8/SVneo cells (immortalized human first-trimester extravillous trophoblast cells) to validate the DEGs and pathways identified in hypoxia-induced primary trophoblast cells. Our results stress the differential expression profiles of mRNAs in hypoxia-induced trophoblast cells, which provide potential pathophysiological mechanisms for preeclampsia.

No association of a Vascular endothelial growth factor A (VEGFA) gene polymorphism with pre-eclampsia among pregnant women in Uganda

BackgroundVascular endothelial growth factor A (VEGFA) is a major angiogenic factor that plays an important role in the formation of blood vessels during embryonic development. VEGFA has been implicated in the pathophysiology of pre-eclampsia (PE), since pre-eclamptic women present with reduced levels of free circulating VEGFA. The 3’ untranslated region (3’-UTR) of the VEGFA gene consists of elements that regulate the transcription and hence expression of the VEGFA protein in circulation. Hence it is suggested that variations thereof could underlie the reduced VEGFA levels observed in pre-eclamptic women. The purpose of this study was to investigate presence of the + 936C/T polymorphism, a common single nucleotide polymorphism (SNP) in the 3’-UTR of the VEGFA gene, and determine its association with PE among pregnant women in Uganda.ResultsThere was no significant difference observed in the allele and genotype frequencies of the + 936C/T 3’ UTR-VEGFA polymorphism between pre-eclamptic and normotensive pregnant women (P > 0.05). Additionally, there was no significant difference in the median plasma levels of free VEGFA among women with the wild type, CT and TT genotypes of the + 936C/T VEGFA polymorphism (median = 0.84 pg/mL (IQR = 0.39–1.41) Vs 1.05 (0.61–1.18) Vs 1.05 (1.05–1.05) respectively, p-value = 0.7161).ConclusionsThese study findings indicate that the + 936C/T 3’ UTR-VEGFA polymorphism had no significant association with increased susceptibility to PE among women in Uganda. Further studies with a larger sample size are recommended.

Preeclampsia pathophysiology and adverse outcomes during pregnancy and postpartum.

Preeclampsia is a disease with far-reaching consequences that extend beyond the immediate postpartum period and have a significant impact later in life. Preeclampsia exerts an effect on most organ systems in the body. These sequelae are mediated in part by the incompletely elucidated pathophysiology of preeclampsia and the associated vascular changes. Current research focuses on unraveling the pathophysiology of preeclampsia with the goal of implementing accurate screening and treatment modalities based on disease development and progression. Preeclampsia causes significant short- and long-term maternal morbidity and mortality, not only in the cardiovascular system but also in other organ systems throughout the body. This impact persists beyond pregnancy and the immediate postpartum period. The goal of this review is to discuss the current understanding of the pathophysiology of preeclampsia as it relates to the adverse health consequences in patients impacted by this disease, along with a brief discussion of ways to improve overall outcomes.

Preeclampsia association of placental nucleotide variations in eNOS, VEGFA, and FLT-1 genes in Latin American pregnant women

IntroductionPreeclampsia is a leading cause of maternal and fetal morbidity in low- and middle-income countries, including those in Latin America. Placental vascular alterations are crucial in the pathophysiology of preeclampsia and few studies have evaluated nucleotide variations on genes associated with vascular regulation in the human placenta. This study aimed to evaluate whether placental nucleotide variations on eNOS, VEGFA, and FLT-1 genes are more frequently associated with preeclampsia in the Latin American population. MethodsThis case-control study included placental tissue from 88 controls and 82 cases that were genotyped through Taqman probes for eNOS, VEGFA, and FLT-1 genes. The intergroup comparisons were analyzed with the Mann-Whitney U test. Genotype and allele frequencies were compared by the X2 test. The association between the nucleotide variants with preeclampsia was evaluated through logistic regression analysis. ResultsA significant association was observed for VEGFA SNV rs2010963 (OR 1.95; CI 95% 1.13–3.37), after adjusting for population substructure. The allele combination T, G, G, C, C, C (rs2070744, rs1799983, rs2010963, rs3025039, rs699947 and rs4769613 respectively), showed a negative association with preeclampsia (OR 0.08; CI 95% 0.01–0.93). results. DiscussionPlacental SNV rs2010963 in the VEGFA gene was a risk factor for preeclampsia, while the allele combination T, G, G, C, C, C may represent potential protective factors for preeclampsia within Latin American women.

The protective effect of magnesium sulfate on placental inflammation via suppressing the NF-κB pathway in a preeclampsia-like rat model.

Abnormal placental inflammation has a role in the pathophysiology of preeclampsia. Magnesium sulfate (MgSO4) has anti-inflammatory properties and is a fetal neuroprotective agent. MgSO4 is often used to treat severe preeclampsia; however, the specificmechanisms of action underlyingthistherapeutic effect remain unclear. The objective of this study was to investigate the effects of MgSO4 (270mg/kg) on placental inflammation in a rat model of lipopolysaccharide (LPS; 1.0µg/kg)-induced preeclampsia. Compared to normal pregnant rats, LPS-treated pregnant rats had higher blood pressure, proteinuria, and expression of the anti-angiogenic factor sFlt-1 and the pro-inflammatory factors interleukin-1β (IL-1β) and IL-12 in placental tissue. LPS-treated pregnant rats had placental insufficiency, poor fetal outcomes, and significantly decreased expression of the anti-inflammatory factors apolipoprotein E (APOE) and IL-10 in placental tissue. MgSO4 treatment had favorable effects on maternal and fetal outcomes. MgSO4 treatment improved placental function by repressing an exaggerated inflammatory response in the placenta and promoting angiogenesis via the NF-κB pathway. These findings suggest MgSO4 has a potential role in the prevention of preeclampsia and in the treatment of mild and moderate preeclampsia.

Metabolomic analysis-identified 2-hydroxybutyric acid might be a key metabolite of severe preeclampsia.

This study set out to determine the key metabolite changes underlying the pathophysiology of severe preeclampsia (PE) using metabolic analysis. We collected sera from 10 patients with severe PE and from 10 healthy pregnant women of the same trimester and analyzed them using liquid chromatography mass spectrometry. A total of 3,138 differential metabolites were screened, resulting in the identification of 124 differential metabolites. Kyoto encyclopedia of genes and genomes pathway analysis revealed that they were mainly enriched in the following metabolic pathways: central carbon metabolism in cancer; protein digestion and absorption; aminoacyl-transfer RNA biosynthesis; mineral absorption; alanine, aspartate, and glutamate metabolism; and prostate cancer. After analysis of 124 differential metabolites, 2-hydroxybutyric acid was found to be the most critical differential metabolite, and its use allowed the differentiation of women with severe PE from healthy pregnant women. In summary, our analysis revealed that 2-hydroxybutyric acid is a potential key metabolite for distinguishing severe PE from healthy controls and is also a marker for the early diagnosis of severe PE, thus allowing early intervention.

NLRP3 inhibition improves maternal hypertension, inflammation, and vascular dysfunction in response to placental ischemia.

Preeclampsia (PE) is a pregnancy-specific hypertensive disorder with end-organ damage that presents after 20 wk of gestation. PE pathophysiology often includes vascular dysfunction and increased inflammation that continues to damage patient health even after PE resolves. Currently, there is no cure for PE beyond delivery of the fetal-placental unit. Previous clinical studies have identified elevated placental NLRP3 expression in patients with PE and suggest NLRP3 as a potential therapeutic target. In this study, we examined the effect of NLRP3 inhibition on PE pathophysiology in the reduced uterine perfusion pressure (RUPP) model rat using MCC950 (20 mg/kg/day) or esomeprazole (3.5 mg/kg/day). We hypothesized that increased NLRP3 in response to placental ischemia impairs anti-inflammatory IL-33 signaling to induce T-helper 17 cell (TH17) and cytolytic NK cell (cNK) activation, which is known to mediate oxidative stress and vascular dysfunction leading to maternal HTN and intrauterine growth restriction. RUPP rats had significantly higher placental NLRP3 expression, maternal blood pressure, fetal reabsorption rate, vascular resistance, oxidative stress, cNKs and TH17s, and decreased IL-33 compared with normal pregnant (NP) rats. NLRP3 inhibition, with either treatment, significantly reduced placental NLRP3 expression, maternal blood pressure, fetal reabsorption rates, vascular resistance, oxidative stress, cNK, and TH17 populations in RUPP rats. Based on our findings, NLRP3 inhibition reduces PE pathophysiology and esomeprazole may be a potential therapeutic for PE treatment.

Setting a stage: Inflammation during preeclampsia and postpartum.

Preeclampsia (PE) is a leading cause of maternal and fetal mortality worldwide. The immune system plays a critical role in normal pregnancy progression; however, inappropriate inflammatory responses have been consistently linked with PE pathophysiology. This inflammatory phenotype consists of activation of the innate immune system, adaptive immune system, and increased inflammatory mediators in circulation. Moreover, recent studies have shown that the inflammatory profile seen in PE persists into the postpartum period. This manuscript aims to highlight recent advances in research relating to inflammation in PE as well as the inflammation that persists postpartum in women after a PE pregnancy. With the advent of the COVID-19 pandemic, there has been an increase in obstetric disorders associated with COVID-19 infection during pregnancy. This manuscript also aims to shed light on the relationship between COVID-19 infection during pregnancy and the increased incidence of PE in these women.

The Role of Peroxisome Proliferator-Activated Receptors in Preeclampsia.

Preeclampsia is a common pregnancy-related hypertensive disorder. Often presenting as preexisting or new-onset hypertension complicated by proteinuria and/or end-organ dysfunction, preeclampsia significantly correlates with maternal and perinatal morbidity and mortality. Peroxisome proliferator-activated receptors (PPARs) are nuclear receptor proteins that regulate gene expression. In order to investigate the role of PPARs in the pathophysiology of preeclampsia, we conducted a literature review using the MEDLINE and LIVIVO databases. The search terms "peroxisome proliferator-activated receptor", "PPAR", and "preeclampsia" were employed and we were able to identify 35 relevant studies published between 2002 and 2022. Different study groups reached contradictory conclusions in terms of PPAR expression in preeclamptic placentae. Interestingly, PPARγ agonists alone, or in combination with well-established pharmaceutical agents, were determined to represent novel, potent anti-preeclamptic treatment alternatives. In conclusion, PPARs seem to play a significant role in preeclampsia.

Preeclampsia: Recent Advances in Predicting, Preventing, and Managing the Maternal and Fetal Life-Threatening Condition.

Preeclampsia accounts for one of the most common documented gestational complications, with a prevalence of approximately 2 to 15% of all pregnancies. Defined as gestational hypertension after 20 weeks of pregnancy and coexisting proteinuria or generalized edema, and certain forms of organ damage, it is life-threatening for both the mother and the fetus, in terms of increasing the rate of mortality and morbidity. Preeclamptic pregnancies are strongly associated with significantly higher medical costs. The maternal costs are related to the extra utility of the healthcare system, more resources used during hospitalization, and likely more surgical spending due to an elevated rate of cesarean deliveries. The infant costs also contribute to a large percentage of the expenses as the babies are prone to preterm deliveries and relevant or causative adverse events. Preeclampsia imposes a considerable financial burden on our societies. It is important for healthcare providers and policy-makers to recognize this phenomenon and allocate enough economic budgets and medical and social resources accordingly. The true cellular and molecular mechanisms underlying preeclampsia remain largely unexplained, which is assumed to be a two-stage process of impaired uteroplacental perfusion with or without prior defective trophoblast invasion (stage 1), followed by general endothelial dysfunction and vascular inflammation that lead to systemic organ damages (stage 2). Risk factors for preeclampsia including race, advanced maternal age, obesity, nulliparity, multi-fetal pregnancy, and co-existing medical disorders, can serve as warnings or markers that call for enhanced surveillance of maternal and fetal well-being. Doppler ultrasonography and biomarkers including the mean arterial pressure (MAP), uterine artery pulsatility index (UtA-PI), and serum pregnancy-associated plasma protein A (PAPP-A) can be used for the prediction of preeclampsia. For women perceived as high-risk individuals for developing preeclampsia, the administration of low-dose aspirin on a daily basis since early pregnancy has proven to be the most effective way to prevent preeclampsia. For preeclamptic females, relevant information, counseling, and suggestions should be provided to facilitate timely intervention or specialty referral. In pregnancies complicated with preeclampsia, closer monitoring and antepartum surveillance including the Doppler ultrasound blood flow study, biophysical profile, non-stress test, and oxytocin challenge test can be arranged. If the results are unfavorable, early intervention and aggressive therapy should be considered. Affected females should have access to higher levels of obstetric units and neonatal institutes. Before, during, and after delivery, monitoring and preparation should be intensified for affected gravidas to avoid serious complications of preeclampsia. In severe cases, delivery of the fetus and the placenta is the ultimate solution to treat preeclampsia. The current review is a summary of recent advances regarding the knowledge of preeclampsia. However, the detailed etiology, pathophysiology, and effect of preeclampsia seem complicated, and further research to address the primary etiology and pathophysiology underlying the clinical manifestations and outcomes is warranted.

Effect of Pregnancy Stages on Changes in Lipid Profiles

Defines Pregnancy is a physiological process occurring among women and female mammals; it usually begins with the process of fertilization of one egg or more, and the evolution of the atom inside the mother's womb is called a fetus or Embryo and continues the development of the fetus inside the mother until the birth. Usually, Pregnancy in women Aly40-36 continues)) almost a week after the end of the last menstrual cycle, more studies on Pregnancy in which women took the biggest in the research and investigation share, compared with studies conducted on female mammals. Pregnancy might result through a traditional male-female partnership or using cutting-edge medical technology. Nevertheless, the fetus grows and develops inside the mother's womb.
 Pregnancy is associated with major changes inside lipid profiles During Pregnancy. This study aimed to determine the level of triglycerides (T.G.), high-density lipoprotein (HDL), total Cholesterol (T.C.), low-density lipoprotein (LDL) and VLDL levels in the third trimester of Pregnancy in Tikrit city pregnant women. Ninety blood samples were taken at various times throughout Pregnancy for this prospective investigation. The analysis of variance was used to look at the data, and a significance level of p 0.05 was used. The results showed that the concentration of Cholesterol increased significantly with the progression of Pregnancy, as it was higher in the second and third stages of Pregnancy compared to the first stage of Pregnancy, while no significant differences were shown in the concentration of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) with the progression of Pregnancy. In contrast, the first and last stages of Pregnancy were significantly superior in the concentration of VLDL and triglycerides (T.G.) compared to the second stage of Pregnancy. Delayed T.G. When high blood pressure in Pregnancy is combined with raised blood T.G. levels, a condition known as preeclampsia may develop. This correlation has the potential to provide light on the pathophysiology of preeclampsia and inform the design of interventions aimed at its early identification and prevention.

Cooperation between NSPc1 and DNA methylation represses HOXA11 expression and promotes apoptosis of trophoblast cells during preeclampsia.

Accumulating evidence has shown that the apoptosis of trophoblast cells plays an important role in the pathogenesis of preeclampsia, and an intricate interplay between DNA methylation and polycomb group (PcG) protein-mediated gene silencing has been highlighted recently. Here, we provide evidence that the expression of nervous system polycomb 1 (NSPc1), a BMI1 homologous polycomb protein, is significantly elevated in trophoblast cells during preeclampsia, which accelerates trophoblast cell apoptosis. Since NSPc1 acts predominantly as a transcriptional inactivator that specifically represses HOXA11 expression in trophoblast cells during preeclampsia, we further show that NSPc1 is required for DNMT3a recruitment and maintenance of the DNA methylation in the HOXA11 promoter in trophoblast cells during preeclampsia. In addition, we find that the interplay of DNMT3a and NSPc1 represses the expression of HOXA11 and promotes trophoblast cell apoptosis. Taken together, these results indicate that the cooperation between NSPc1 and DNMT3a reduces HOXA11 expression in preeclampsia pathophysiology, which provides novel therapeutic approaches for targeted inhibition of trophoblast cell apoptosis during preeclampsia pathogenesis.

Association between serum hypovitaminosis D and preeclampsia: A nested case-control study

Background: Preeclampsia is a major complication of pregnancy and a major cause of perinatal and maternal morbidity and mortality. Vitamin D deficiency has been implicated in the aetiology and pathophysiology of preeclampsia. However, there is no uniformity in the findings of previous studies on the association between vitamin D and preeclampsia. Aims and Objectives: The study is aimed at determining the association between preeclampsia and maternal vitamin D deficiency. Materials and Methods: This nested case-control study was conducted among 158 pregnant women (78 preeclamptic women and 80 controls) with singleton pregnancies. Case participants were women with preeclampsia. The controls were matched pregnant women without preeclampsia. Their serum vitamin D levels were determined. Statistics: Continuous data was analysed using T-test. The statistical significance was inferred at p- value ≤0.05. Results: The prevalence of hypovitaminosis D in our study was 7.0% overall. The proportion of women with hypovitaminosis D was not significantly different between preeclampsia group and control group (7.7% vs 6.3% respectively; p=0.76). The mean serum concentration of vitamin D in the preeclamptic group was lower than that in the control group, however, the difference was not statistically significant (118.8±17.4nmol/L vs 129.0±19.7nmol/L, p=0.17). There was a weak association between gestational age and the level of serum vitamin D in both groups (r= 0.062 and r= -0.13 respectively). Conclusions: Hypovitaminosis D is not significantly associated with preeclampsia when compared with control. However, there was a weak association between gestational age and the level of serum vitamin D in both groups.