Search Results (761)

The widespread production and poor management of plastic waste have led to the pervasive presence of microplastics (MPs) in environmental and biological systems. Among various polymers, polyethylene (PE) is the most widely produced plastic globally, primarily due to its use in single-use packaging. Its persistence in ecosystems and resistance to degradation processes result in the continuous formation of PE-derived MPs. These particles have been detected in human biological matrices, including blood, lungs, placenta, and even the brain, raising increasing concerns about their bioavailability and potential health effects. Once internalized, PE MPs can interact with cellular membranes, induce oxidative stress, inflammation, and apoptosis, and interfere with epigenetic regulatory pathways. In vitro studies on epithelial, immune, and neuronal cells reveal concentration-dependent cytotoxicity, mitochondrial dysfunction, membrane disruption, and activation of pro-inflammatory cytokines. Moreover, recent findings suggest that PE MPs can induce epithelial-to-mesenchymal transition (EMT), senescence, and epigenetic dysregulation, including altered expression of miRNAs and DNA methyltransferases. These cellular changes highlight the potential role of MPs in disease development, especially in cardiovascular, metabolic, and possibly cancer-related conditions. Despite growing evidence, no standardized method currently exists for quantifying MPs in human samples, complicating comparisons across studies. Further, MPs can carry harmful additives and environmental contaminants such as bisphenols, phthalates, dioxins, and heavy metals, which enhance their toxicity. Global estimates indicate that humans ingest and inhale tens of thousands of MPs particles each year, yet long-term human research remains limited. Given these findings, it is crucial to expand research on PE MP toxicodynamics and to establish regulatory policies to reduce their release. Promoting alternative biodegradable materials and improved waste management practices will be vital in decreasing human exposure to MPs and minimizing potential health risks. Full article

Fine particulate matter (PM2.5) emitted by wood smoke is a significant environmental pollutant associated with oxidative stress and hypoxia. These conditions can disrupt placental function by altering the expression of key nutrient transporters, such as glucose transporter 1 (GLUT1) and sodium-dependent vitamin C transporter 2 (SVCT2), which are essential for fetal development. This study evaluates the effects of pregestational and gestational exposure to PM2.5 on GLUT1 and SVCT2 expression in the rat placenta. Pregnant Sprague–Dawley rats were exposed to either filtered air (FA) or non-filtered air (NFA) containing PM2.5 from wood combustion in a controlled exposure system. Four experimental groups were established: FA/FA (control), FA/NFA (gestational exposure), NFA/FA (pregestational exposure), and NFA/NFA (continuous exposure). Immunofluorescence and confocal microscopy were used to quantify the expression of GLUT1 and SVCT2 in the placental labyrinth zone. Statistical analyses were performed using Kruskal–Wallis and post hoc Dunn’s test (p < 0.05). Gestational exposure to PM2.5 (FA/NFA) significantly reduced GLUT1 and SVCT2 expression, compromising glucose transport and antioxidant protection in the placenta. Pregestational exposure (NFA/FA) induced a compensatory increase in SVCT2 expression, suggesting an adaptive response to oxidative stress. Continuous exposure (NFA/NFA) resulted in GLUT1 redistribution within the syncytiotrophoblast and decreased membrane localization, potentially impairing glucose uptake. PM2.5 exposure disrupts the expression and localization of GLUT1 and SVCT2 in the placenta, with differential effects depending on the timing of exposure. The gestational phase appears to be particularly vulnerable, as reduced GLUT1 and SVCT2 levels may impair fetal nutrition and antioxidant defense. These findings underscore the need for preventive measures to mitigate air pollution-related risks during pregnancy. Full article

Rift Valley Fever Virus (RVFV) is an arbovirus that predominantly affects sheep, goats, and cattle, causing epizootics in livestock and epidemics in humans. Infection in pregnant livestock leads to high abortion rates and neonatal mortality. In humans, RVFV usually causes a self-limiting febrile illness, but severe forms can develop, such as hepatitis, hemorrhage, encephalitis, and death. In addition, the association between RVFV infection during pregnancy and miscarriages or stillbirths has been documented. RVFV is transmitted by a range of mosquito species, and, due to the diffusion of these insects, the virus has spread in several world regions, making possible the risk of a public health emergency. Nevertheless, research remains limited and cellular pathology is still poorly characterized. This work aimed to fill some knowledge gaps on the comprehension of RVFV pathogenesis. For this purpose, transmission electron microscopy (TEM) was used to analyze cellular modifications associated with RVFV morphogenesis in four human cell lines (HuH-7, LAN-5, A549, and HTR-8/SVneo) derived from liver, brain, lung, and placenta. Our results showed that all four cell lines are permissive to RVFV infection and highlighted differences in the cytopathogenesis associated with the cell type. These findings could have important implications in understanding disease mechanisms and developing antiviral strategies. Full article

Human chorionic gonadotropin (hCG) is a pregnancy biomarker, and five forms of this hormone are involved in female physiological regulation. β-core fragment hCG (bcf-hCG) is a fragment of hCG whose biological role in female reproduction has not been completely elucidated. This study aimed to investigate its role in embryo implantation and maintenance of a pregnancy-supportive environment. We analyzed the protein expression pattern of bcf-hCG in the intrauterine environment during early pregnancy by performing western blotting and immunohistochemistry with a monoclonal anti-bcf-hCG antibody. We performed a cell proliferation assay in the presence of bcf-hCG compared with intact hCG. We conducted an ex vivo study by performing intrauterine injection of bcf-hCG or intact hCG in mice. Endometrial thickness was measured using histological methods, and uterine gene and protein expression were analyzed following intrauterine injection of bcf-hCG. We evaluated the effect of bcf-hCG on embryo implantation in the uterus. bcf-hCG was highly abundant in the placenta and epithelial stromal glands of the uterine endometrium during early pregnancy and significantly induced proliferation of a stromal epithelial cell line. Intrauterine injection of bcf-hCG induced expression of specific genes and proteins, including homeobox A10, for embryo implantation and placental development. Upon embryo transfer, the implantation rate of bcf-hCG-treated embryos was higher than that of control embryos. In conclusion, bcf-hCG plays a role in the proliferation of glandular epithelial cells in the endometrium and placenta during early pregnancy. Therefore, bcf-hCG is an early-phase pregnancy biomarker that maintains the initial phase of pregnancy. Full article

The insulin-like growth factor (IGF) system regulates implantation, placental development, and angiogenesis in eutherian mammals. However, little is known about the changes in this system in equine placenta (chorioallantois; CA) and the endometrium (EN) during pregnancy, or the relationship to vascular endothelial growth factor (VEGF) expression. The current study investigated the expression of the IGF system components, namely the ligands (IGF1 and IGF2), their receptors (IGF1R, IGF2R, and INSR), and their binding proteins (IGFBPs and IGF2BPs) in equine CA at 45 days, 4, 6, 10, and 11 months of gestational age (GA) and immediately postpartum (PP), and in equine EN at 4, 6, 10, and 11 months GA. IGF1 immunolocalization and serum concentrations were also evaluated across gestation. IGF1 mRNA expression in CA increased from day 45 to peak at 6 months and then gradually declined to reach a nadir in PP samples. This profile correlated positively with the VEGF expression profile (r = 0.62, p = 0.001). In contrast, IGF2 expression in CA was not correlated with VEGF (p = 0.14). Interestingly, IGF2 mRNA was more abundant in equine CA than IGF1 (p < 0.05) throughout gestation. Among the IGFBPs investigated in CA, the expression of IGFBP2 and IGF2BP2 was highly abundant (p < 0.05) at day 45 compared to other GAs. Conversely, mRNA expression for IGFBP3 and IGFBP5 was more abundant (p < 0.05) in PP than at all investigated GAs. Immunohistochemistry revealed that IGF1 is localized in the equine chorionic epithelium (cytoplasm and nucleus). IGF1 serum concentrations peaked at 9 months and declined to their lowest levels PP. In conclusion, this study demonstrates a positive correlation between IGF1 and VEGF expression in equine CA during gestation, suggesting that the IGF system plays a crucial role in placental angiogenesis by regulating VEGF. Full article

The windowpane oyster (Placuna placenta) is common in coastal areas of the Philippines, thriving in brackish waters. Its shells underpin the local craft industries. While its meat is edible, only small amounts are consumed locally, most going to waste. Utilization of this potential nutrient source is hindered by the lack of information concerning its organic and mineral content, the possible presence of heavy metal ions, and the risk of microbial pathogens. We report extensive analysis of the meat from Placuna placenta, harvested during three different seasons to account for potential variations. This comprises proximate analysis, mineral, antioxidant, and microbial analyses. While considerable seasonal variation was observed, the windowpane oyster was found to be a rich source of protein, fats, minerals, and carbohydrates, comparing well with the meats of other shellfish and land animals. Following pre-cooking (~90 °C, 25–30 min), the standard local method for food preparation, no viable E. coli or Salmonella sp. were detected. Mineral content was broadly similar to that reported in fish, although iron, zinc, and copper were more highly represented, nevertheless, heavy metals were below internationally acceptable levels, with the exception of one of three samples, which was slightly above the only current standard, FSANZ. Whether the arsenic was in the safer organic form, which is commonly the case for shellfish, or the more toxic inorganic form remains to be established. This and the variation of arsenic over time will need to be considered when developing food products. Overall, the meat of the windowpane oyster is a valuable food resource and its current (albeit low-level) use should lower any barriers to its acceptance, making it suitable for commercialization. The present data support its development for high-value food products in urban markets. Full article

Congenital Chagas disease (CCD) is caused when Trypanosoma cruzi crosses the placental barrier during pregnancy and reaches the fetus, which can lead to serious consequences in the developing fetus. Current treatment is carried out with nifurtimox or benznidazole, but their effectiveness is limited, and they cause side effects, requiring the search for new therapeutic strategies. In this sense, many studies have demonstrated the potential of different compounds of the Copaifera genus in the control of parasitic diseases. Here, we aimed to evaluate the effect of oleoresin (OR) and leaf hydroalcoholic extract (LHE) of Copaifera multijuga on Trypanosoma cruzi infection in human villous trophoblast cells (BeWo line) and human placenta explants. Treatment with both compounds reduced invasion, proliferation, and release of trypomastigotes. Furthermore, OR and LHE affected the trypomastigotes and amastigote morphology, compromising their ability to invade and proliferate in BeWo cells, respectively. Also, treatment with OR decreased ROS production in infected BeWo cells, while LHE induced an increase. In addition, both compounds induced pro-inflammatory and anti-inflammatory cytokine production. In human placental explants, both compounds also decreased T. cruzi infection, in addition to inducing the production of pro-inflammatory cytokines. Thus, both OR and LHE of C. multijuga control T. cruzi infection at the human maternal–fetal interface, highlighting the possible therapeutic potential of these compounds for the treatment of CCD. Full article

Syphilis, which is caused by Treponema pallidum, remains one of the most common congenital infection worldwide and has tremendous consequences for the mother and her developing foetus if left untreated. The complexity of the exposure to this pathogen extends beyond the well-established clinical manifestations, as it can profoundly affect placental histomorphology. This study aimed to compare T. pallidum-exposed placental villi structures with healthy placentae at term to evaluate the histomorphological differences using stereology. In this case-control study conducted at term (38 weeks ± 2 weeks), 78 placentae were collected from the hospital delivery suites, comprising 39 cases (T. pallidum-exposed) and 39 controls (non-exposed), who were gestational age-matched with other potential confounders excluded. Blood samples from the umbilical vein and placental basal plate were tested for syphilis, using rapid diagnostic test (RDT) kits for T. pallidum (TP) antibodies (IgG and IgM) to classify placentae as exposed to T. pallidum (cases) and non-exposed (controls). Tissue sections were prepared and stained with haematoxylin and eosin, and the mean volume densities of syncytial knots, foetal capillaries, syncytial denuded areas, and intervillous spaces were estimated using stereological methods. Statistical analysis was performed to compare the mean values between the case and control groups. Stereological assessment revealed significant differences between the T. pallidum-exposed and non-exposed groups with regard to syncytial knots (p < 0.0001), syncytial denudation (p < 0.0001), and foetal capillaries (p < 0.0001), but no significant difference in the intervillous space was found (p = 0.1592). Therefore, our study shows, for the first time, that the histomorphology of human placental villi appears to be altered by exposure to T. pallidum. It will, therefore, be interesting to determine whether these changes in the placental villi translate into long-term effects on the baby. Full article

Background: Fatty acid status during the perinatal period is important for optimal offspring growth and development. Objectives: We aimed to test the association between maternal fatty acid (FA) intake during the third trimester of pregnancy and the FA composition of placental phospholipids, a marker of maternal fatty acid status. Methods: This cohort study was performed on 54 mothers participating in the PREOBE study. Maternal dietary intake was assessed with prospective 7-day food diaries at 34 weeks of gestation. Placenta samples were collected immediately after delivery and phospholipid FA was quantified with established methods. Data were analyzed with Pearson correlations and linear regression models, with adjustment for confounding factors. Results: Total energy intake was 2019 ± 527 kcal/d (mean ± SD) and total fat intake of the mothers was 87 ± 35 g/day. Myristic, stearic, oleic, and α-linolenic acid intakes were modestly correlated with placental percentages, with r-values ≤ 0.33. Only docosahexaenoic (DHA) acid intake (%-energy, %-fat, and g/d) showed r-values > 0.4 for the correlation with placenta phospholipids. Intake of other fatty acids, including arachidonic acid, was not associated with the placenta percentage. Linear regression models considering confounders showed only dietary DHA intake significant associations. Total fat intake did not interfere with the association of DHA intake with placental incorporation. Conclusions: DHA and arachidonic acid are enriched in the placenta, but only placental DHA content seems modifiable by maternal dietary DHA intake. Full article

Background: The worldwide prevalence of FGR is about 13% and can lead to various adverse perinatal outcomes, including preterm birth, stillbirth, and neonatal mortality. Hypoxia-Inducible Factor-1 (HIF-1) is an important regulator of oxygen homeostasis in humans and is crucial for placental development. The aim of this study is to determine the pattern of HIF-1A expression in placenta, and to correlate its association with preeclampsia, fetal growth restriction and adverse perinatal outcomes. Methods: This study comprised a total of 158 cases with 42 cases of mother having babies with fetal growth restriction (FGR), 39 cases of mother with preeclampsia (PE), 35 cases of mother with preeclampsia and fetal growth restriction and 42 controls. The expression of HIF-1A was evaluated in various placental cell types, including cytotrophoblasts, syncytiotrophoblasts, fetal endothelial cells, maternal endothelial cells, and decidual cells. Results: The expression of HIF-1A in placental decidual cells of mother with FGR (21/42, 50%, p < 0.0001), PE (25/39, 64.1%, p < 0.0001) and PE with FGR (12/35, 34.3%, p < 0.0001) were significantly increased compared to controls (1/42). Intriguingly, HIF-1A expression was significantly reduced in the placental cytotrophoblasts and syncytiotrophoblasts of mother with PE and FGR (2/35, 5.7%) compared to PE alone (11/39, 28.2%) (p = 0.0142). Conclusions: We found that increased HIF-1A expression in the nuclei of decidual cells was observed in the mothers of babies with FGR, both with and without PE. While HIF-1A expression in the cytotrophoblasts and syncytiotrophoblasts was significantly reduced between mothers with PE and mothers with PE and FGR. This suggests HIF-1A expression might play a role in the pathogenesis of FGR. Full article

The suppressive regulator of cell fusion, suppressyn, is specifically expressed in the human placenta and is thought to play a crucial role in trophoblast fusion or syncytialization. Previous studies have suggested that alterations in its expression are associated with aberrant placental development, such as the immature placental morphology observed in Down syndrome, and may contribute to the pathogenesis of fetal growth restriction. While syncytialization in trophoblasts is an essential process for normal placental development, the precise molecular causes of its dysregulation remain poorly understood. In the present study, we aimed to elucidate the potential contribution of genomic variation to the loss of suppressyn function, extending previous analyses of expression abnormalities in perinatal disorders. Through sequence analysis, (1) we identified six polymorphisms within the coding region of the suppressyn gene, and (2) discovered that certain deletions and specific amino acid substitutions result in a complete loss of suppressyn-mediated inhibition of cell fusion. Although these mutations have not yet been reported in disease-associated genomic databases, our findings suggest that comprehensive genomic studies of perinatal and other disorders may reveal pathogenic variants of suppressyn, thereby uncovering novel genetic contributions to placental dysfunction. It is also anticipated that these findings might direct the development of therapeutic strategies targeting loss-of-function mutations. Full article

Background: Prematurely born newborns with low birth weight constitute a group of patients who require special care from the first days of life. Prematurity and low birth weight affect about 13.4 million infants. Risk factors include placental disorders but also factors related to the mother, such as smoking, alcohol drinking, drug use, malnutrition, or certain diseases. It is imperative to educate women of reproductive age (15–49) about the basic factors influencing embryonic development, such as oral health, diet, medicine intake, and harmful habits. Even though most women are aware of the negative impact of harmful habits on the fetus, still too little attention is paid to oral health in pregnant women. Poor oral health may influence the well-being of the future mother, as well as of the child. Therefore, women of reproductive age and those who are pregnant must have adequate knowledge on this subject. The aim of this study was to assess the knowledge of Polish women of reproductive age (15–49) regarding oral health during pregnancy, including the impact of dental treatment, oral hygiene, and maternal oral conditions on pregnancy outcomes and the health of the newborn. Materials and Methods: This was a cross-sectional study of 508 women, in the reproductive age, whose age ranged from 18 to 49 years old. The surveys were conducted from April 2020 to November 2020. The questionnaire was originally developed based on the available literature and consisted of seven sections: basic information, general health and habits, pregnancy status and dental care, knowledge of treatment options during pregnancy, oral health status and its association with the risk of preterm birth, prematurity and the child’s oral health, and breastfeeding and oral development. Results: After excluding incomplete questionnaires, a total of 499 questionnaires were included in the analysis. Women participating in the study had a fairly good understanding of the impact of oral health on the fetus and the role of breastfeeding in the development of the stomatognathic system (from 50% to 70% correct answers). However, even though most respondents had completed higher education (344/68.94%), their knowledge of oral health, preterm birth, and low birth weight was very limited (including the impact of inflammation on the intrauterine development of the child or bacteria and transfer across the placenta). In these sections, the percentage of correct answers ranged from less than 20% to 50%. When analyzing knowledge by age, education, number of births, and place of residence, the highest levels of knowledge were observed among respondents with higher education, particularly those aged 27–32. Conclusions: Respondents had a fairly good understanding of the general impact of oral health during pregnancy and recognition of the importance of breastfeeding for infants. However, their knowledge about the impact of bacteria and inflammation in the mother’s oral cavity on prematurity and low birth weight was limited. Therefore, educating women of reproductive age and pregnant women on this topic is essential, as it may help reduce the adverse consequences of prematurity. Full article

Obesity affects approximately 30% of pregnancies worldwide and is one of the leading metabolic disorders among pregnant women. Maternal obesity is often associated with placental dysfunction and structural alterations, which increase the risk of developing complications. Efflux transporters, including P-glycoprotein (P-gp), may impact placental function and fetal development. Consequently, our research examined the effects of obesity on P-glycoprotein expression in both a rat model and human placental tissue. P-gp expression was measured by RT-PCR and Western blot techniques in human and rat placental tissues. Moreover, we further characterized the high-fat and high-sugar diet (HFHSD)-induced gestational obesity rat model by measuring tissue weights. Significant decreases were observed in fetal, placental, and uterus weights in the obese animals near the end of pregnancy. In obese rats, mRNA and protein expression of placental P-gp showed a reduction on gestation days 15, 20, and 22. A similar P-gp reduction was observed in the term placenta in obese women in mRNA and protein levels. We hypothesize that the reduced expression of P-gp may heighten the susceptibility of both the fetus and placenta to P-gp substrates. This alteration could potentially result in an increased risk of pregnancy complications and obesity-related drug contraindications linked to P-gp transport during pregnancy. Full article

Background/Objectives: Gestational diabetes mellitus (GDM) is a common metabolic disorder in pregnant women. It can lead to several complications, such as preterm delivery, macrosomia, or metabolic disorders in newborns. Studies have revealed morphological and transcriptional differences between the placentas of patients with GDM and women with normal glucose tolerance. Sirtuins (SIRTs) are nicotinamide adenine dinucleotide-dependent deacetylases that interact with and regulate the activity of numerous proteins. However, little is known about their role in the pathogenesis of GDM. This study was performed to analyze the placental expression of SIRTs and investigate their correlations with clinical parameters. Methods: GDM was diagnosed based on the 75 g oral glucose tolerance test in accordance with the criteria developed by the International Association of Diabetes and Pregnancy Study Groups. Placental tissues were collected, and the expression of SIRT1,-3,-4 and a reference gene (β-2 microglobulin) was analyzed. Results: The placental expression of SIRT1 and SIRT3 was elevated in women with GDM. However, there was no significant difference in SIRT4 expression between women with GDM and those with normal glucose tolerance. Furthermore, we found no significant correlations between SIRT1, SIRT3, and SIRT4 expression and clinical parameters. Conclusions: The findings of this study demonstrate elevated expression of SIRT1 and SIRT3 in the placentas of women with GDM. Further studies are required to confirm our observations and demonstrate the precise role of these enzymes in GDM. Full article

Background: Obesity during pregnancy is associated with an elevated risk of severe COVID-19, including higher rates of maternal complications, intensive care admission, and adverse neonatal outcomes. The impact of combination of SARS-CoV-2 infection and maternal obesity in placental pathology has not been properly investigated. Aim: To compare the histopathological changes in the placenta induced by active SARS-CoV-2 infection in obese and non-obese patients. Methods: This retrospective cohort study included human placentas from non-obese women and pre-gestationally obese women with active SARS-CoV-2 infection (SARS and OB+SARS, respectively), and placentas from non-obese women and pre-gestationally obese women without SARS-CoV-2 infection (control and OB, collected in the post- and pre-pandemic periods, respectively). Results: A higher (50%) occurrence of ischemic injury and subchorionic fibrin deposits and a 15× higher risk of occurrence of these lesions were found in the OB+SARS group, in relation to control. In contrast, a 10% lower risk of developing chorangiosis in the OB+SARS group than the OB group was observed. Conclusions: An increased risk of lesions related to both maternal and fetal malperfusion and ischemic injury and a lower risk for chorangiosis exist in placentas from obese women affected by SARS-CoV-2 infection. Importantly, these differences were not observed in placentas from non-obese women. Full article