Objective: To analyze endocan-1, a biomarker of vascular endothelial related pathologies, and the placental growth factor (PlGF), an angiogenic factor and a placental dysfunction marker in patients with preeclampsia (PE).
Methods: Case-control study conducted at Hospital São Lucas, in the city of Porto Alegre, Brazil. Endocan-1 and PlGF levels were quantified in the maternal plasma using the MagPlexTH-C microsphere system (MAGPIX System, Luminex, Austin, Texas, US) and evaluated through analysis of covariance (ANCOVA) and adjusted by body mass index (BMI), gestational age and maternal age. To estimate the difference between the groups, the mean ratio (MR) and the 95% confidence interval (95%CI) were calculated. The Pearson correlation test was used to establish any association between endocan-1 and PlGF levels. The null hypothesis was rejected when < 0.05.
Results: The group of patients was composed by normotensive ( = 67) patients and patients with PE ( = 50). A negative correlation between endocan-1 and the PlGF was noted in the entire normotensive group (linear correlation coefficient [r] = -0.605; < 0.001), as well as in the PE group (r = -0.545; < 0.001).
Conclusion: Endocan-1 levels are increased in patients with PE, and are inversely correlated with PlGF levels. We suggest that it is important to analyze angiogenic and proinflammatory molecules concomitantly in women with PE to better understand the pathophysiology of the disease. Both molecules are strong candidates for PE biomarkers, and future studies will examine any mechanisms connecting these factors in PE.
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http://dx.doi.org/10.1055/s-0038-1670713 | DOI Listing |
Arch Gynecol Obstet
January 2025
Faculty of Medicine and Health Sciences, Tel Aviv University, Tel Aviv, Israel.
Purpose: To quantify the separation between maternal blood cell-free (cf)DNA markers in preeclampsia and unaffected pregnancies and compare with existing markers. This approach has not been used in previous studies.
Methods: Comprehensive systematic literature search of PubMed to identify studies measuring total cfDNA, fetal cf(f)DNA or the fetal fraction (FF) in pregnant women.
Histochem Cell Biol
January 2025
Medical Histology and Cell Biology Department, Faculty of Medicine, Mansoura University, Mansoura, 35516, Egypt.
Gestational diabetes mellitus (GDM) significantly disrupts placental structure and function, leading to complications such as intrauterine growth restriction (IUGR) and preeclampsia. This study aimed to investigate the effects of GDM on placental histology, angiogenesis, and oxidative stress, as well as evaluate metformin's protective role in mitigating these changes. A total of 60 pregnant Sprague-Dawley rats were divided into four groups: control, metformin-treated, GDM, and GDM with metformin.
View Article and Find Full Text PDFJ Physiol
January 2025
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
The mechanisms that drive placental dysfunction in pregnancies complicated by hypoxia and fetal growth restriction remain poorly understood. Changes to mitochondrial respiration contribute to cellular dysfunction in conditions of hypoxia and have been implicated in the pathoaetiology of pregnancy complications, such as pre-eclampsia. We used bespoke isobaric hypoxic chambers and a combination of functional, molecular and imaging techniques to study cellular metabolism and mitochondrial dynamics in sheep undergoing hypoxic pregnancy.
View Article and Find Full Text PDFSequestration of parasites in the placental vasculature causes increased morbidity and mortality in pregnant compared to non-pregnant patients in malaria- endemic regions. In this study, outbred pregnant CD1 mice with semi allogeneic fetuses were infected with transgenic or mock-inoculated by mosquito bite at either embryonic day (E) 6 (first trimester-equivalent) or 10 (second trimester- equivalent) and compared with non-pregnant females. -infected mosquitoes had greater biting avidity for E10 dams than uninfected mosquitoes, which was not apparent for E6 dams nor non-pregnant females.
View Article and Find Full Text PDFEnviron Pollut
January 2025
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR; Arkansas Children's Nutrition Center, Little Rock, AR.
The placenta is crucial for fetal development, is affected by PFAS toxicity, and evidence is accumulating that gestational PFAS perturb the epigenetic activity of the placenta. Gestational PFAS exposure can adversely affect offspring, yet individual and cumulative impacts of PFAS on the placental epigenome remain underexplored. Here, we conducted an epigenome-wide association study (EWAS) to examine the relationships between placental PFAS levels and DNA methylation in a cohort of mother-infant dyads in Arkansas (N=151).
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