Coordinated expression of TNFα- and VEGF-mediated signaling components by placental macrophages in early and late pregnancy

Павлов, О. В.; Niauri, Dariko A.; Selutin, A.V.; Selkov, S. A.

doi:10.1016/j.placenta.2016.04.008

Cited by 18 publications

(6 citation statements)

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“…In normal pregnancy, there is an increase in placental secretion of TNF-α and vascular endothelial growth factor (VEGF), which is believed to promote normal placental angiogenesis and growth (Pavlov et al 2016). It has recently been discovered that TNF-α stimulates production of a member of the VEGF family, placental growth factor (PlGF), in trophoblasts (Kato et al 2016).…”

Section: Tnf-αmentioning

confidence: 99%

“…It has recently been discovered that TNF-α stimulates production of a member of the VEGF family, placental growth factor (PlGF), in trophoblasts (Kato et al 2016). TNF-α is a key regulator of implantation and trophoblast function in the first trimester and has been shown to induce apoptosis in cultured trophoblast cells (Knöfler et al 2000; Pavlov et al 2016; Siwetz et al 2016). Thus, TNF-α appears to be important for trophoblast turnover and differentiation and overall placental development, a concept supported by the increasing maternal serum TNF-α levels across gestation (Christian and Porter 2014).…”

Section: Tnf-αmentioning

confidence: 99%

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Effects of maternal obesity on placental function and fetal development

2017

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Obesity has reached epidemic proportions and pregnancies in obese mothers have increased risk for complications including gestational diabetes, hypertensive disorders, preterm birth and caesarian section. Children born to obese mothers are at increased risk of obesity and metabolic disease and are susceptible to develop neuropsychiatric and cognitive disorders. Changes in placental function not only play a critical role in the development of pregnancy complications but may also be involved in linking maternal obesity to long-term health risks in the infant. Maternal adipokines i.e., interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), leptin and adiponectin link maternal nutritional status and adipose tissue metabolism to placental function. Adipokines and metabolic hormones have direct impact on placental function by modulating placental nutrient transport. Nutrient delivery to the fetus is regulated by a complex interaction between insulin signaling, cytokine profile and insulin responsiveness, which is modulated by adiponectin and IL-1β. In addition, obese pregnant women are at risk for hypertension and preeclampsia with reduced placental vascularity and blood flow, which would restrict placental nutrient delivery to the developing fetus. These sometimes opposing signals regulating placental function may contribute to the diversity of short and long-term outcomes observed in pregnant obese women. This review focuses on the changes in adipokines and obesity-related metabolic hormones, how these factors influence placental function and fetal development to contribute to long-term metabolic and behavioral consequences of children born to obese mothers.

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Section: Tnf-αmentioning

confidence: 99%

Section: Tnf-αmentioning

confidence: 99%

Effects of maternal obesity on placental function and fetal development

2017

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“…As an alternative to studying responses to whole pathogens, several groups have investigated HBC responses to individual pathogen-associated molecular patterns (PAMPs) including lipopolysaccharide (LPS) (6,69,104,(109)(110)(111)(112)(113)(114)(115), merozoite surface protein 1 (MSP1) (116), polyinosinic:polycytidylic acid (PIC) and peptidoglycan (PGN) (110,114), and Imiquimod and FSL-1 stimulation (110) (Table 5). HBCs were isolated mainly from third trimester placentas (n=9 studies) (6,69,109,(111)(112)(113)(114)(115)(116), with only three studies using HBCs from the first or second trimester (6,110,112).…”

Section: Hbc Responses To Pathogen Associated Molecular Patterns (Pamps)mentioning

confidence: 99%

Placental Macrophage (Hofbauer Cell) Responses to Infection During Pregnancy: A Systematic Scoping Review

et al. 2022

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BackgroundCongenital infection of the fetus via trans-placental passage of pathogens can result in severe morbidity and mortality. Even without transmission to the fetus, infection of the placenta itself is associated with pregnancy complications including pregnancy loss and preterm birth. Placental macrophages, also termed Hofbauer cells (HBCs), are fetal-origin macrophages residing in the placenta that are likely involved in responding to placental infection and protection of the developing fetus. As HBCs are the only immune cell present in the villous placenta, they represent one of the final opportunities for control of infection and prevention of passage to the developing fetus.Objective and RationaleThe objective of this review was to provide a systematic overview of the literature regarding HBC responses during infection in pregnancy, including responses to viral, bacterial, and parasitic pathogens.MethodsPubMed and Scopus were searched on May 20th, 2021, with no limit on publication date, to identify all papers that have studied placental macrophages/Hofbauer cells in the context of infection. The following search strategy was utilized: (hofbauer* OR “hofbauer cells” OR “hofbauer cell” OR “placental macrophage” OR “placental macrophages”) AND [infect* OR virus OR viral OR bacteri* OR parasite* OR pathogen* OR LPS OR “poly(i:c)” OR toxoplasm* OR microb* OR HIV)].Outcomes86 studies were identified for review. This included those that investigated HBCs in placentas from pregnancies complicated by maternal infection and in vitro studies investigating HBC responses to pathogens or Pathogen-Associated Molecular Patterns (PAMPs). HBCs can be infected by a variety of pathogens, and HBC hyperplasia was a common observation. HBCs respond to pathogen infection and PAMPs by altering their transcriptional, translational and secretion profiles. Co-culture investigations demonstrate that they can replicate and transmit pathogens to other cells. In other cases, they may eliminate the pathogen through a variety of mechanisms including phagocytosis, cytokine-mediated pathogen elimination, release of macrophage extracellular traps and HBC-antibody-mediated neutralization. HBC responses differ across gestation and may be influenced by pre-existing immunity. Clinical information, including gestational age at infection, gestational age of the samples, mode of sample collection and pregnancy outcome were missing for the majority of studies.

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“…Importantly the effects of BPA on the placenta appear to vary depending on the stage of the pregnancy and consistent with a latency in final outcomes. During early gestation, BPA induced increase in inflammation and oxidative stress, reduced levels of TNF, a cytokine with role in promoting placental function (Jaattela et al, 1988;Basu et al, 2016;Pavlov et al, 2016), and reduced bioavailability of IGFs may be the main drivers for reduced placental efficiency and fetal weight. During the mid-gestation, lag in action of increased expression of antioxidants observed during early-gestation and large magnitude albeit non-significant mid-gestational increase in both IGFs and its receptors may have aided in circumventing the increase in IGFBPs leading to restoration of placental efficiency and fetal weight.…”

Section: Linking Bpa Induced Placental Changes With Placental Efficiency and Fetal Growthmentioning

confidence: 99%

Developmental programming: Prenatal bisphenol A treatment disrupts mediators of placental function in sheep

et al. 2020

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Gestational Bisphenol A (BPA) exposure is associated with low birth weight. We hypothesized that the low birth weight is the consequence of reduced placental efficiency and a function of BPAinduced inflammatory, oxidative, lipotoxic, angiogenic, steroidal and fibrotic changes involving epigenetic alterations. Placentomes were collected during early (day 65) and mid (day 90) gestation (term ~147 days) from control and BPA (gestational day 30-90)-treated pregnant sheep. BPA treatment: reduced placental efficiency and fetal weight; increased interleukin 8, lipid peroxidation marker, antioxidants, aromatase, 17 alpha-hydroxylase, estrogen receptor 2, insulin like growth factor (IGF) 2 receptor and IGF binding proteins (IGFBP), and histone deacetylase 1 and 2; reduced tumor necrosis factor alpha and IGF1 receptor at early gestation (Day 65). Gestational BPA-induced mid-gestational changes include: reduced angiogenic factor hypoxia inducible factor 1 alpha; increased IL1beta, oxidative stress markers, triglyceride, 17alpha hydroxylase, IGFBP 1, DNA methyltransferase 3A and histone deacetylase 1. These findings indicate that gestational BPA, either acting directly or by altering steroidal input, produces early/ mid-gestational-specific epigenetic changes culminating in placental disruptions at several levels, in keeping with time-specific/time-lagged pregnancy-associated changes in placental efficiency and fetal weight. The reduced early-gestational placental efficiency may be a function of increased inflammation/oxidative stress and reduced IGF bioavailability with the mid-gestational restoration of placental efficiency likely driven by improved IGF bioavailability and the time-lagged response to antioxidant increase. This compensation, the result of time-lagged response to increases in negative mediators of placental function must have failed with pregnancy advancement to explain the low birthweight outcome.

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Coordinated expression of TNFα- and VEGF-mediated signaling components by placental macrophages in early and late pregnancy

Cited by 18 publications

References 47 publications

Effects of maternal obesity on placental function and fetal development

Effects of maternal obesity on placental function and fetal development

Placental Macrophage (Hofbauer Cell) Responses to Infection During Pregnancy: A Systematic Scoping Review

Developmental programming: Prenatal bisphenol A treatment disrupts mediators of placental function in sheep

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