Evidence for episodic GnRH-modulated hCG secretion by placental tissue in vitro

1989 ◽  
Vol 120 (3_Suppl) ◽  
pp. S103 ◽  
Author(s):  
W. E. MERZ ◽  
C. ERLEWEIN ◽  
P. LICHT ◽  
T. O. F. WAGNER
Keyword(s):  
Placental Tissue ◽  
Hcg Secretion

scholarly journals Human tissue mast cells are an inducible reservoir of persistent HIV infection

Blood ◽  
2007 ◽  
Vol 109 (12) ◽  
pp. 5293-5300 ◽  
Author(s):  
J. Bruce Sundstrom ◽  
Jane E. Ellis ◽  
Gregory A. Hair ◽  
Arnold S. Kirshenbaum ◽  
Dean D. Metcalfe ◽  
...  
Keyword(s):  
Mast Cells ◽  
Highly Active Antiretroviral Therapy ◽  
Mononuclear Cells ◽  
Tissue Injury ◽  
Allergic Inflammation ◽  
Placental Tissue ◽  
Latently Infected ◽  
Tissue Compartments

AbstractWe have proposed that, unlike other HIV-vulnerable cell lineages, progenitor mast cells (prMCs), cultured in vitro from undifferentiated bone marrow–derived CD34+ pluripotent progenitors (PPPs), are susceptible to infection during a limited period of their ontogeny. As infected prMCs mature in culture, they lose expression of viral chemokine coreceptors necessary for viral entry and develop into long-lived, latently infected mature tissue mast cells (MCs), resistant to new infection. In vivo recruitment of prMCs to different tissue compartments occurs in response to tissue injury, growth, and remodeling or allergic inflammation, allowing populations of circulating and potentially HIV-susceptible prMCs to spread persistent infection to diverse tissue compartments. In this report, we provide in vivo evidence to confirm this model by demonstrating that HIV-infected women have both circulating prMCs and placental tissue MCs (PLMCs) that harbor inducible infectious HIV even after highly active antiretroviral therapy (HAART) during pregnancy. Furthermore, infectious virus, capable of infecting alloactivated fetal cord blood mononuclear cells (CBMCs), could be induced in isolated latently infected PLMCs after weeks in culture in vitro. These data provide the first in vivo evidence that tissue MCs, developed from infected circulating prMCs, comprise a long-lived inducible reservoir of persistent HIV in infected persons during HAART.

Abstract 207: C-Reactive Protein Signaling via Neurokinin B Receptor Contributes to the Pathophysiology of Preeclampsia

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Nicholas Parchim ◽  
Wei Wang ◽  
Chen Liu ◽  
Athar Siddiqui ◽  
Rodney Kellems ◽  
...  
Keyword(s):  
Placental Tissue ◽  
Protein Signaling ◽  
Post Translational Modification ◽  
C Reactive Protein ◽  
Neurokinin B ◽  
Bacterial Membranes ◽  
Reactive Protein ◽  
Nk3 Receptor ◽  
Invasion Index

Introduction: C-Reactive Protein (CRP) is an important immunomodulatory molecule. Early studies have indicated that CRP is elevated in preeclamptic patient sera, but its function remains unclear. CRP is known to bind with phosphocholine (PC) of bacteria membrane to kill bacteria by triggering innate immune response. Phosphocholination is a post-translational modification mediated by PC transferase, an enzyme reported expressed only in two tissues, including placenta and testis. Recent studies identified that Neurokinin B (NKB), a known, placenta-enriched pathogenic molecule for preeclampsia (PE), is phosphocholinated. This modification increases its stability, preferentially activates NK3 receptor (NK3R) and promotes PE features. Given CRP can bind to PC on bacterial membranes, the role that phosphocholination plays is a mystery. In light of NKB, being phosphocholinated in the endoplasmic reticulum and signals via the NK3R in the pathogenesis of PE, we feel that elevated CRP may be associated with NKB and contributes to the pathophysiology of PE via NK3R activation. Results: ELISA results show that CRP is significantly elevated in PE vs. control sera_65 ug/mL vs. 10 ug/ml; p<0.0001. Western blot analysis reveals that CRP, NKB, and NK3R are significantly increased in PE vs. control placental tissue. Immunohistochemistry studies indicate that all of these three molecules are abundant in syncytiotrophoblast cells. Co-immunoprecipitation demonstrates an interaction between CRP and NKB. In vitro , we provide the first evidence that CRP decreased the invasion of trophoblast cells from 0.7 ± 0.06 to 0.06 ± 0.001 invasion index; p<0.005, while treatment with SB222200 ameliorates shallow invasion from 0.28 ± 0.09 to 0.55 ± 0.07 invasion index; p<0.05. Significantly, infusion of CRP into pregnant mice induces hypertension (169.152 ± 14.7 mmHg vs. 141.916 ± 6.93 mmHg; p<0.05) and proteinuria (28.78 ± 13.56 mg albumin/μg Cr vs. 13.87 ± 3.277 mg albumin/μg Cr; p<0.05). Conclusion: Our findings demonstrate elevated CRP contributes to PE and NKB/NK3R is a new mechanism underlying CRP-mediated shallow invasion and disease development. These studies suggest novel pathogenic biomarkers and innovative therapies for PE.

scholarly journals Omega-3 Fatty Acid-Derived Resolvin D2 Regulates Human Placental Vascular Smooth Muscle and Extravillous Trophoblast Activities

2019 ◽  
Vol 20 (18) ◽  
pp. 4402 ◽  
Author(s):  
Arzu Ulu ◽  
Prakash K. Sahoo ◽  
Ana G. Yuil-Valdes ◽  
Maheswari Mukherjee ◽  
Matthew Van Ormer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Placental Tissue ◽  
Cell Types ◽  
Extravillous Trophoblast ◽  
Protective Effects ◽  
Omega 3 Fatty Acids ◽  
Omega 3

Omega-3 fatty acids are important to pregnancy and neonatal development and health. One mechanism by which omega-3 fatty acids exert their protective effects is through serving as substrates for the generation of specialized pro-resolving lipid mediators (SPM) that potently limit and resolve inflammatory processes. We recently identified that SPM levels are increased in maternal blood at delivery as compared to umbilical cord blood, suggesting the placenta as a potential site of action for maternal SPM. To explore this hypothesis, we obtained human placental samples and stained for the SPM resolvin D2 (RvD2) receptor GPR18 via immunohistochemistry. In so doing, we identified GPR18 expression in placental vascular smooth muscle and extravillous trophoblasts of the placental tissues. Using in vitro culturing, we confirmed expression of GPR18 in these cell types and further identified that stimulation with RvD2 led to significantly altered responsiveness (cytoskeletal changes and pro-inflammatory cytokine production) to lipopolysaccharide inflammatory stimulation in human umbilical artery smooth muscle cells and placental trophoblasts. Taken together, these findings establish a role for SPM actions in human placental tissue.

Genotype and fetal size affect maternal­–fetal amino acid status and fetal endocrinology in Large White×Landrace and Meishan pigs

2013 ◽  
Vol 25 (2) ◽  
pp. 439 ◽  
Author(s):  
Cheryl J. Ashworth ◽  
Margaret O. Nwagwu ◽  
Harry J. McArdle
Keyword(s):  
Amino Acid ◽  
Plasma Concentrations ◽  
Placental Tissue ◽  
Maternal Plasma ◽  
Plasma Amino Acid ◽  
Large White ◽  
Fetal Plasma ◽  
Acid Status ◽  
Fetal Size

This study compared maternal plasma amino acid concentrations, placental protein secretion in vitro and fetal body composition and plasma amino acid and hormone concentrations in feto–placental units from the smallest and a normally-sized fetus carried by Large White × Landrace or Meishan gilts on Day 100 of pregnancy. Compared with Large White × Landrace, Meishan placental tissue secreted more protein and Meishan fetuses contained relatively more fat and protein, but less moisture. Fetal plasma concentrations of insulin, triiodothryonine, thyroxine and insulin-like growth factor (IGF)-II were higher in Meishan than Large White × Landrace fetuses. In both breeds, fetal cortisol concentrations were inversely related to fetal size, whereas concentrations of IGF-I were higher in average-sized fetuses. Concentrations of 10 amino acids were higher in Large White × Landrace than Meishan gilts, while glutamine concentrations were higher in Meishan gilts. Concentrations of alanine, aspartic acid, glutamic acid and threonine were higher in Meishan than Large White × Landrace fetuses. Average-sized fetuses had higher concentrations of asparagine, leucine, lysine, phenylalanine, threonine, tyrosine and valine than the smallest fetus. This study revealed novel genotype and fetal size differences in porcine maternal–fetal amino acid status and fetal hormone and metabolite concentrations.

Human placental cytochrome P450 and quinone reductase enzyme induction in relation to maternal smoking

1995 ◽  
Vol 7 (6) ◽  
pp. 1521 ◽  
Author(s):  
AG Boden ◽  
PG Bush ◽  
MD Burke ◽  
DR Abramovich ◽  
P Aggett ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Maternal Smoking ◽  
High Performance ◽  
Smoking Habit ◽  
Placental Tissue ◽  
Maternal Plasma ◽  
Quinone Reductase ◽  
Polycyclic Aromatic ◽  
Plasma Cotinine

Components of cigarette smoke such as cadmium and polycyclic aromatic hydrocarbons have been shown to induce quinone reductase (QR) activity in placental explants. This study examines the relationship of maternal smoking habit and maternal plasma cotinine concentration with the activities in vitro of both QR and the cytochrome P450 (CYP1A) marker ethoxyresorufin O-deethylase (EROD) in placental tissue. Maternal plasma samples were taken at Week 34 of gestation, and placental tissues were obtained at term. Plasma cotinine concentrations were determined by high-performance liquid chromatography. Trophoblast cytosolic QR and microsomal EROD activities were measured by resazurin reduction and ethoxyresorufin O-dealkylation respectively. QR activity was inhibited 70% by a mixture of dicoumarol (1 microM) and rutin (20 microM). Plasma cotinine concentrations correlated significantly (P < 0.001) with both declared smoking rate (r = 0.67, N = 37) and placental EROD activity (r = 0.63, N = 36), but not with QR activity, whether measured as total QR activity or specifically as either DT-diaphorase or carbonyl reductase. It is concluded that smoking up to 40 cigarettes per day induces EROD but does not affect QR activity in the placenta at term.

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