Increased expression levels of E-cadherin, cytokeratin 18 and 19 observed in preeclampsia were not correlated with disease severity

Li, X.L.; Dong, Xin; Xue, Yan; Li, C.F.; Gou, Wei; Chen, Q.

doi:10.1016/j.placenta.2014.04.010

Cited by 30 publications

(28 citation statements)

References 27 publications

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“…The dysregulation of this progress is associated with pregnancy complications (17,18). Previous studies have reported that e-cadherin expression is markedly increased in placenta tissues from patients with Pe compared with controls, whereas the expression levels of n-cadherin and Snail are decreased (30)(31)(32). on the basis of these previous studies, the present study investigated the effects of mir-335-5p on JeG-3 cell migration and key eMT markers.…”

Section: Discussionmentioning

confidence: 86%

ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

Shao

et al. 2019

Mol Med Report

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differential expression of microrna (mir)-335-5p, a key tumor suppressor, has been detected in pre-eclampsia (Pe) placentas. However, the role of mir-335-5p in the pathogenesis of Pe and the factor modulating its aberrant expression remain unknown. The present study used JeG-3 cells in vitro to investigate these mechanisms. The role of mir-335-5p in proliferation, apoptosis and migration of JeG-3 cells was investigated using MTT, annexin V-FiTc/Pi, Transwell migration and wound healing assays, respectively. mir-335-5p expression levels were analyzed using reverse transcription-quantitative Pcr. The expression levels of e-cadherin, N-cadherin, Snail, specificity protein 1 (Sp1) and p53 were assessed using western blot analysis. cell viability analysis was performed using the cell counting Kit-8 assay. The intracellular reactive oxygen species (roS) levels were detected using a 2,7-dichlorodihydrofluorescein diacetate assay. The present results suggested that mir-335-5p did not affect the proliferation or apoptotic rate of JeG-3 cells. overexpression of miR-335-5p significantly inhibited the migration of JEG-3 cells, decreased the expression levels of Sp1, n-cadherin and Snail, and increased e-cadherin expression. Sp1 silencing produced similar results in JeG-3 cells. H 2 o 2 significantly increased the intracellular roS levels and mir-335-5p expression, whereas n-acetyl-cysteine pretreatment prior to H 2 o 2 treatment reversed the increases in mir-335-5p expression. Knockdown of p53 significantly decreased the expression levels of mir-335-5p in JeG-3 cells and in H 2 o 2-treated cells. The present results suggested that mir-335-5p expression levels in trophoblast cells could be increased by roS in a p53-dependent manner, leading to the downregulation of Sp1 and subsequent inhibition of epithelial to mesenchymal transition and cell migration. The present results may provide novel evidence on the etiology of Pe.

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Section: Discussionmentioning

confidence: 86%

ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

Shao

et al. 2019

Mol Med Report

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“…The image shown represents a single representative example of 10 separate experiments C o n t r o l P E 120 kD E-cadherin 42 kD β-actin E-cadherin, which is a classical cell-cell adhesion molecule, is expressed in villous cytotrophoblasts and its expression and location are associated with the morphology of trophoblasts and are important for healthy placental development (16). The expression of E-cadherin has been shown to be elevated in preeclamptic placentas (17). It has been reported that an elevation of the expression of E-cadherin promotes the proliferation of cytotrophoblasts and inhibits their differentiation into syncytiotrophoblasts in PE (18).…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of E-cadherin, Endothelin-1, and CD68 in Preeclamptic Placentas

İrtegün¹,

Tekin²,

Alpayci³

2016

Erciyes Med J

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Objective: Preeclampsia (PE) is a complex pregnancy-specific disorder characterized by the onset of hypertension and proteinuria in the second trimester of pregnancy. The pathogenesis of PE still remains unknown. Revealing the specific proteins involved in placental functions is important for a better understanding of the pathogenesis of PE. In this study, we aimed to investigate the expression levels of E-cadherin, endothelin-1, and CD68 in both preeclamptic and normal placentas. Materials and Methods:In this study, placentas after birth at 35-38 weeks were included. Ten preeclamptic placentas and 10 normal placentas were used. The expression levels of E-cadherin, endothelin-1, and CD68 were measured by western blot.Results: It was observed that the expression of E-cadherin and endothelin-1 was not at detectable levels in normal placentas; however, E-cadherin and endothelin-1 were observed to be highly expressed in preeclamptic placentas. In addition, the expression of CD68 was found to be markedly increased in preeclamptic placentas in comparison to control placentas. Conclusion:The increased expression of E-cadherin, endothelin-1, and CD68 may play an important role in impaired trophoblast invasion, endothelial dysfunction, and inadequate spiral remodeling, which are key factors involved in the pathogenesis of PE.

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“…The cytotrophoblasts between densities of 1.049 g/ml and 1.062 g/ml were collected and plated at 2 Â 10 4 cells/well in a 96-well plate or 1 Â 10 6 cells per well in a 12-well plate or 2 Â 10 6 cells per well in a 6-well plate for culture at 37 in 5% CO 2 and 95% air in DMEM containing 10% fetal calf serum (FCS) (Gibco) and 1% antibiotics (Gibco). Freshly-isolated cytotrophoblasts were incubated for 0, 24, 48 and 72 h and at each time point cells were then treated with 0.1 mM PFOS for 24 h. This was carried out to examine the effect of PFOS on the expression of syncytialization related markers, including E-cadherin, a classical cellecell adhesion molecule, which is expressed in villous cytotrophoblasts, but is lost when cytotrophoblasts syncytialize into syncytiotrophoblasts [21], and syncytin, a crucial mediator involved in the syncytialization of cytotrophoblasts [22]. Previous studies have shown that maximal syncytialization is achieved three days after plating [23].…”

Section: Preparation and Culture Of Human Placental Trophoblasts And mentioning

confidence: 99%

Reduction of progesterone, estradiol and hCG secretion by perfluorooctane sulfonate via induction of apoptosis in human placental syncytiotrophoblasts

Zhang

Wang

et al. 2015

Placenta

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Increased expression levels of E-cadherin, cytokeratin 18 and 19 observed in preeclampsia were not correlated with disease severity

Cited by 30 publications

References 27 publications

ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

ROS/p53/miR‑335‑5p/Sp1 axis modulates the migration and epithelial to mesenchymal transition of JEG‑3 cells

Increased Expression of E-cadherin, Endothelin-1, and CD68 in Preeclamptic Placentas

Reduction of progesterone, estradiol and hCG secretion by perfluorooctane sulfonate via induction of apoptosis in human placental syncytiotrophoblasts

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