Expressions of steroid receptors and Ki67 in first-trimester decidua and chorionic villi exposed to levonorgestrel used for emergency contraception

2009 ◽  
Vol 91 (4) ◽  
pp. 1420-1423 ◽  
Author(s):  
Chun-Xia Meng ◽  
Li-Nan Cheng ◽  
Parameswaran Grace Luther Lalitkumar ◽  
Lin Zhang ◽  
Hui-Juan Zhang ◽  
...  
2012 ◽  
Vol 1822 (11) ◽  
pp. 1660-1670 ◽  
Author(s):  
Stefania Gessi ◽  
Stefania Merighi ◽  
Angela Stefanelli ◽  
Prisco Mirandola ◽  
Alessandra Bonfatti ◽  
...  

Author(s):  
Yang Yang ◽  
Jiashu Li ◽  
Yingying Zhou ◽  
Wen Dai ◽  
Weiping Teng ◽  
...  

Elevated thyroid stimulating hormone (TSH) is associated with an increased risk of spontaneous abortion (SA); however, the associated mechanism remains unclear. This study aimed to investigate the expression of microRNAs (miRNAs) and pathogenesis in the chorionic villi of TSH > 2.5 mIU/L-related SA patients. The chorionic villi were collected from pregnant women in the first trimester with TSH > 2.5 mIU/L with or without SA, as well as TSH < 2.5 mIU/L with or without SA to determine the level of miRNA expression. Differentially expressed miRNAs were confirmed by qRT-PCR in a total of 92 subjects. Cell counting kit-8 (CCK8), wound healing, transwell assays, and Western blotting were used to measure cellular biological functions and related protein in HTR-8/SVneo cells. The potential mechanisms were determined using a Luciferase reporter assay and rescue experiment. Compared with normal pregnant women, miR-17-5p was decreased and zinc finger protein 367 (ZNF367) was upregulated in the chorionic villi of TSH > 2.5 mIU/L-related SA patients. Using HTR-8/SVneo cells, we demonstrated that elevated TSH inhibited miR-17-5p expression, as well as trophoblast migration and invasion. The overexpression of miR-17-5p targeted and inhibited ZNF367 expression promoting the biological function of trophoblasts. Further studies confirmed that ZNF367 interference partially reversed the biological function of the miR-17-5p inhibitor on HTR-8/SVneo cells. Taken together, our results showed that miR-17-5p promoted biological function of trophoblasts by suppressing ZNF367.


2003 ◽  
Vol 285 (6) ◽  
pp. R1453-R1460 ◽  
Author(s):  
S. D. Appleton ◽  
G. E. Lash ◽  
G. S. Marks ◽  
K. Nakatsu ◽  
J. F. Brien ◽  
...  

Although hypoxia induces heme oxygenase (HO)-1 mRNA and protein expression in many cell types, recent studies in our laboratory using human placental tissue have shown that a preexposure to hypoxia does not affect subsequent HO enzymatic activity for optimized assay conditions (20% O2; 0.5 mM NADPH; 25 μM methemalbumin) or HO-1 protein content. One of the consequences of impaired blood flow is glucose deprivation, which has been shown to be an inducer of HO-1 expression in HepG2 hepatoma cells. The objective of the present study was to test the effects of a 24-h preexposure to glucose-deprived medium, in 0.5 or 20% O2, on HO protein content and enzymatic activity in isolated chorionic villi and immortalized HTR-8/SVneo first-trimester trophoblast cells. HO protein content was determined by Western blot analysis, and microsomal HO enzymatic activity was measured by assessment of the rate of CO formation. HO enzymatic activity was increased ( P < 0.05) in both placental models after 24-h preexposure to glucose-deficient medium in 0.5 or 20% O2. Preexposure (24 h) in a combination of low O2 and low glucose concentrations decreased the protein content of the HO-1 isoform by 59.6% ( P < 0.05), whereas preexposure (24 h) to low glucose concentration alone increased HO-2 content by 28.2% in chorionic villi explants ( P < 0.05). In this preparation, HO enzymatic activity correlated with HO-2 protein content ( r = 0.825). However, there was no correlation between HO-2 protein content and HO enzymatic activity in HTR-8/SVneo trophoblast cells preexposed to 0.5% O2 and low glucose concentration for 24 h. These findings indicate that the regulation of HO expression in the human placenta is a complex process that depends, at least in part, on local glucose and oxygen concentrations.


Radiology ◽  
1984 ◽  
Vol 151 (1) ◽  
pp. 159-162 ◽  
Author(s):  
A V Cadkin ◽  
N A Ginsberg ◽  
E Pergament ◽  
Y Verlinski

1988 ◽  
Vol 11 (2) ◽  
pp. 123-130 ◽  
Author(s):  
L. Poenaru ◽  
L. Castelnau ◽  
A-M. Besançon ◽  
H. Nicolesco ◽  
S. Akli ◽  
...  

1996 ◽  
Vol 149 (2) ◽  
pp. 249-258 ◽  
Author(s):  
S McCracken ◽  
J E Layton ◽  
S C Shorter ◽  
P M Starkey ◽  
D H Barlow ◽  
...  

Abstract The development of the placenta is dependent upon the regulated proliferation, invasion and differentiation of trophoblast. Expression of cytokines at the feto-maternal interface suggests that these molecules may participate in placentation. The expression of granulocyte-colony stimulating factor (G-CSF) and G-CSF receptor (G-CSFR) during the development of the human placenta was studied by immunohistochemistry using an anti-G-CSF monoclonal antibody (mAb) and two novel anti-G-CSFR mAbs. G-CSF was present in the stroma of fetal chorionic villi and maternal decidual tissues throughout pregnancy. G-CSFR was detected at high levels in fetal first and third, but not second trimester placental tissues. Staining for G-CSFR was undetectable in maternal decidual tissue from all gestational stages. In first trimester tissues, staining for placental G-CSFR was strongest in differentiated syncytiotrophoblast and invasive, extravillous cytotrophoblast, and weak staining was evident in undifferentiated cytotrophoblast. Immunohistochemical data suggesting temporal regulation of G-CSFR were corroborated by Western blotting and amplification by reverse transcription and PCR of G-CSFR mRNA. These data suggested that expression of G-CSFR in the human placenta is regulated both temporally and spatially, and that placental G-CSF is involved in paracrine regulation, and indicate a role for G-CSF and G-CSFR in trophoblast growth or function during placentation. Journal of Endocrinology (1996) 149, 249–258


2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Elizabeth Ann L. Enninga ◽  
Regan N. Theiler

Lymphocytic choriomeningitis virus (LCMV) is a rodent disease that can be transmitted to humans. A majority of persons infected with LCMV have only minor symptoms; however, it can cross the placental barrier during pregnancy and cause congenital defects in the fetus. Some viral infections early in gestation are hypothesized to lead to worse outcomes compared to those acquired during late gestation; however, LCMV has not been studied in this context. In the present study, differences in immunomodulation between the first- and third-trimester placental explants infected with LCMV were measured. LCMV replication was observed in the first-trimester chorionic villi, but not in term. The term placenta exhibited a robust innate immune response to infection by LCMV, marked by induction of ifn-α, il-6, and tnf-α gene expression which was not seen in the first-trimester explants. Cytokine secretion was also only seen in term explants. The results indicate that the first-trimester and term placentas differ in their permissiveness for LCMV infection, inversely correlating with the innate antiviral responses. This has implications for developing effective mechanisms that protect the fetus from infection based on stage of development.


2013 ◽  
Vol 33 (5) ◽  
pp. 502-508 ◽  
Author(s):  
Francesca R. Grati ◽  
Francesca Malvestiti ◽  
Beatrice Grimi ◽  
Elisa Gaetani ◽  
Anna Maria Di Meco ◽  
...  

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