Betamethasone reverses AVP-induced dysfunction in trophoblast cells

2022 ◽  
Vol 226 (1) ◽  
pp. S443-S444
Author(s):  
Christopher D. Clark ◽  
Donna A. Santillan ◽  
Mark K. Santillan
Keyword(s):  
1985 ◽  
Vol 54 (02) ◽  
pp. 438-441 ◽  
Author(s):  
K Dalaker ◽  
E Haug ◽  
H Prydz

SummaryTrophoblasts from murine placenta synthesize thromboplastin in the absence of inducing agents and a functional complement system, nor is the rate or level of synthesis enhanced by inducers. A serum factor which is destroyed/removed by addition of oxalate and subsequent dialysis appears to enhance the ability of trophoblasts to synthesize thromboplastin.


2019 ◽  
Vol 35 (6) ◽  
pp. 80-86
Author(s):  
E.A. Knyazeva ◽  
S.V. Nikulin ◽  
A.Yu. Khristichenko ◽  
V.A. Petrov ◽  
A. Turchinovich ◽  
...  

The model of the placental barrier based on the human choriocarcinoma cell line BeWo b30 allows studying the effect of hypoxia on trophoblast cells. The effect of the oxyquinoline derivative inhibiting HIF-prolyl hydroxylases was studied on this model. Inhibition of these enzymes leads to an increase in the HIF-1α subunit in the cytoplasm, mimicking the cell response to hypoxia. Incubation of the cells with the drug at a concentration of 10 uM for 24 h did not affect the paracellular transport, but reduced the transport of glucose through the cell barrier. The transcriptome analysis after the exposure with oxyquinoline derivative revealed a decreased expression of the KIAA1217 gene and its intronic gene MIR603, which encodes microRNA hsa-miR-603. The expression of the target gene of this miRNA, CCND1 encoding cyclin D1, after oxyquinoline derivative exposition increased significantly, which may indicate a potential microRNA-mRNA regulatory mechanism in the response of trophoblast cells to hypoxia. BeWo b30, placenta, hypoxia, oxyquinoline, barrier, microRNA, cyclin The study was performed with the equipment of the «Postgenomic and Metabolomic Methods of Study in Molecular Biology» Common Use Center (BioClinicum Scientific and Technical Center). The study was supported by the Ministry of Education and Science of the Russian Federation in the framework of the Federal Targeted Program for Research and Development in Priority Areas of Advancement of the Russian Scientific and Technological Complex for 2014-2020 (Project no. RFMEFI58817X0007).


2021 ◽  
Vol 22 (13) ◽  
pp. 7226
Author(s):  
Violeta Stojanovska ◽  
Aneri Shah ◽  
Katja Woidacki ◽  
Florence Fischer ◽  
Mario Bauer ◽  
...  

Cold shock Y-box binding protein-1 (YB-1) coordinates several molecular processes between the nucleus and the cytoplasm and plays a crucial role in cell function. Moreover, it is involved in cancer progression, invasion, and metastasis. As trophoblast cells share similar characteristics with cancer cells, we hypothesized that YB-1 might also be necessary for trophoblast functionality. In samples of patients with intrauterine growth restriction, YB-1 mRNA levels were decreased, while they were increased in preeclampsia and unchanged in spontaneous abortions when compared to normal pregnant controls. Studies with overexpression and downregulation of YB-1 were performed to assess the key trophoblast processes in two trophoblast cell lines HTR8/SVneo and JEG3. Overexpression of YB-1 or exposure of trophoblast cells to recombinant YB-1 caused enhanced proliferation, while knockdown of YB-1 lead to proliferative disadvantage in JEG3 or HTR8/SVneo cells. The invasion and migration properties were affected at different degrees among the trophoblast cell lines. Trophoblast expression of genes mediating migration, invasion, apoptosis, and inflammation was altered upon YB-1 downregulation. Moreover, IL-6 secretion was excessively increased in HTR8/SVneo. Ultimately, YB-1 directly binds to NF-κB enhancer mark in HTR8/SVneo cells. Our data show that YB-1 protein is important for trophoblast cell functioning and, when downregulated, leads to trophoblast disadvantage that at least in part is mediated by NF-κB.


2021 ◽  
Vol 22 (12) ◽  
pp. 6260
Author(s):  
Hyun-Jung Lee ◽  
Seung Mook Lim ◽  
Hee Yeon Jang ◽  
Young Ran Kim ◽  
Joon-Seok Hong ◽  
...  

Preterm labor (PTL) is one of the obstetric complications, and is known to be associated with abnormal maternal inflammatory response and intrauterine inflammation and/or infection. However, the expression of specific miRNAs associated with PTL is not clear. In this study, we performed combination analysis of miRNA array and gene array, and then selected one miRNA (miR-373-3p) and its putative target genes (CD44 and RDX) that exhibited large expression differences in term and PTL placentas with or without inflammation. Using qRT-PCR and luciferase assays, we confirmed that miR-373-3p directly targeted CD44 and RDX. Overexpression of miR-373-3p reduced the migration and invasion of trophoblast cells, while inhibition of miR-373-3p restored the migration and invasion abilities of trophoblast cells. Finally, we validated the expression of miR-373-3p and its target genes in clinical patients’ blood. miR-373-3p was increased in PTL patients’ blood, and was the most expressed in PTL patients’ blood with inflammation. In addition, by targeting the miR-373-3p, CD44 and RDX was decreased in PTL patients’ blood, and their expression were the lowest in PTL patients’ blood with inflammation. Taken together, these findings suggest that miR-373-3p and its target genes can be potential biomarkers for diagnosis of PTL.


2019 ◽  
Vol 316 (4) ◽  
pp. C481-C491 ◽  
Author(s):  
Yalan Xu ◽  
Lili Sui ◽  
Bintao Qiu ◽  
Xiuju Yin ◽  
Juntao Liu ◽  
...  

The inadequate trophoblast invasion is associated with the development of preeclampsia (PE). Considering that annexin A4 (ANXA4) enhances tumor invasion, we aimed to explore the functional role of ANXA4 in trophoblast cells and to examine the underlying mechanism. ANXA4 expression in PE placentas was analyzed using immunohistochemistry and Western blotting. Cell proliferation, invasion, and apoptosis were determined using a MTT assay, Transwell assay, and flow cytometry, respectively. The expression levels of matrix metalloproteinase (MMP)-2, MMP-9, phosphoinositide 3-kinase (PI3K), Akt, phosphorylated (p)-Akt, and phosphorylated endothelial nitric oxide synthase (p-eNOS) were detected by Western blotting. Placentas were prepared for pathological examination using hematoxylin and eosin staining and apoptosis determination using the TUNEL method. Expression of ANXA4, PI3K, p-Akt and p-eNOS was downregulated in human PE placentas and PE placenta-derived extravillous cytotrophoblasts (EVCTs). Furthermore, ANXA4 overexpression promoted cell proliferation and invasion, inhibited cell apoptosis, and upregulated protein expression of PI3K, p-Akt, and p-eNOS in human trophoblast cells HTR-8/SVneo and JEG-3. By contrast, ANXA4 knockdown exerted the opposite effects. Furthermore, inhibition of the PI3K/Akt pathway by LY294002 abrogated the ANXA4 overexpression-mediated effects on trophoblast behavior. Furthermore, eNOS knockdown abrogated the ANXA4 overexpression-induced promotion of cell invasion and MMP2/9 expression. Additionally, in N-nitro-l-arginine methyl ester (l-NAME)-induced PE rats, ANXA4 overexpression alleviated PE progression, accompanied by an increase in expression of PI3K, p-Akt, and p-eNOS in rat placentas. Our findings demonstrate that ANXA4 expression is downregulated in PE. ANXA4 may promote trophoblast invasion via the PI3K/Akt/eNOS pathway.


Biology ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 238
Author(s):  
Malgorzata Kloc ◽  
Ahmed Uosef ◽  
Jacek Z. Kubiak ◽  
Rafik M. Ghobrial

Human placenta formation relies on the interaction between fused trophoblast cells of the embryo with uterine endometrium. The fusion between trophoblast cells, first into cytotrophoblast and then into syncytiotrophoblast, is facilitated by the fusogenic protein syncytin. Syncytin derives from an envelope glycoprotein (ENV) of retroviral origin. In exogenous retroviruses, the envelope glycoproteins coded by env genes allow fusion of the viral envelope with the host cell membrane and entry of the virus into a host cell. During mammalian evolution, the env genes have been repeatedly, and independently, captured by various mammalian species to facilitate the formation of the placenta. Such a shift in the function of a gene, or a trait, for a different purpose during evolution is called an exaptation (co-option). We discuss the structure and origin of the placenta, the fusogenic and non-fusogenic functions of syncytin, and the mechanism of cell fusion. We also comment on an alleged danger of the COVID-19 vaccine based on the presupposed similarity between syncytin and the SARS-CoV-2 spike protein.


2007 ◽  
Vol 197 (6) ◽  
pp. S172
Author(s):  
Kathryn Drennan ◽  
Adrian Platts ◽  
Amelia Linneman ◽  
Graham Johnson ◽  
Stephen Krawetz

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