Macrophage-stimulating protein is decreased in severe preeclampsia and regulates the biological behavior of HTR-8/SVneo trophoblast cells

Placenta ◽  
2021 ◽  
Vol 103 ◽  
pp. 33-42
Author(s):  
Hongqin Chen ◽  
Yanping Zhang ◽  
Jin Jia ◽  
Jie Ren ◽  
Hongbiao Yu ◽  
...  
2020 ◽  
Vol 745 ◽  
pp. 139919
Author(s):  
Wenhui Zha ◽  
Shuang Guan ◽  
Ning Liu ◽  
Yang Li ◽  
Yuan Tian ◽  
...  

2018 ◽  
Vol 26 (7) ◽  
pp. 954-960 ◽  
Author(s):  
Ling Huang ◽  
Yuanyuan Li ◽  
Chunhui Wang ◽  
Na Li ◽  
Yue Hou ◽  
...  

Collapsin response mediator protein 1 (CRMP-1) is widely expressed in the nervous system and has tumor suppressive effects. Our previous studies have demonstrated that CRMP-1 was expressed in the trophoblasts of the whole stage of pregnancy with significantly increasing expression in the placenta of early-onset preeclampsia. Preeclampsia, especially early onset, is strongly associated with the dysfunction of trophoblast including proliferation, apoptosis, migration, and invasion. In this study, we found an inhibitory effect of CRMP-1 on proliferation, migration, invasion, and an enhanced effect on apoptosis in human trophoblast cell lines HTR-8/SVneo and JEG-3 by MTT assay, colony formation assay, cell viability assay, caspase 3/7 activity assay, scratch wound assay, and Matrigel Transwell assay. Overexpression of CRMP-1 in trophoblast cells led to downregulate expression of matrix metalloproteinase 2 and 9. The expression of CRMP-1 was detected by real-time quantitative polymerase chain reaction and Western blot analysis. Thus, we suggested that CRMP-1 might have implications for the pathogenesis of preeclampsia by regulating the biological behavior of trophoblast cells.


Reproduction ◽  
2020 ◽  
Vol 160 (1) ◽  
pp. 21-29
Author(s):  
Rongli Wang ◽  
Li Zou

A successful pregnancy crucially depends on well-regulated extravillous trophoblast migration and invasion. Maternally expressed gene 3 (MEG3) is a long noncoding RNA that plays an important role in regulating trophoblast cells cell function. As previously reported, the expression of MEG3 was reduced in preeclampsia, and downregulation of MEG3 could suppress trophoblast cells migration and promote its apoptosis. However, the downstream regulatory mechanism of MEG3 remains unknown. As reported, MEG3 could inhibit cell proliferation in endometrial carcinoma by regulating Notch signaling. Our previous studies have demonstrated that Notch1 is downregulated in preeclampsia and that inhibiting the expression of Notch1 could promote trophoblast cell apoptosis. Therefore, this study was designed to investigate the role of MEG3 and its the relationship with Notch1 in trophoblasts. In this study, the mRNA expression levels of both MEG3 and Notch1 were decreased in preeclampsia placenta (n = 15) compared to the normal samples (n = 15). Exogenous upregulation and downregulation of MEG3 in HTR8/SVneo cells were performed to investigate the role of MEG3 in cell biological behavior and its effects on Notch1 expression. The results showed that MEG3 enhancement promoted trophoblast cell migration and invasion and inhibited cell apoptosis. Downregulation of MEG3 elicited the opposite results. Associated factors, such as matrix metalloproteinases 2 (MMP2), BAX, and Bcl-2, were examined at the mRNA and protein levels. Our study demonstrated that MEG3 could regulate Notch1 expression to modulate trophoblast cell migration, invasion, and apoptosis, which may represent the molecular mechanism of poor placentation during preeclampsia.


Ob Gyn News ◽  
2011 ◽  
Vol 46 (5) ◽  
pp. 8
Author(s):  
SUSAN LONDON

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.


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