Transcription factors E2F1 and E2F3 are expressed in placenta but do not regulate MMP14

Kaitu’u-Lino, Tu’uhevaha J; Hastie, Roxanne; Cannon, Ping; Nguyen, Huy; Lee, S.; Hannan, Natalie J.; Tong, Stephen

doi:10.1016/j.placenta.2015.06.007

Cited by 9 publications

(4 citation statements)

References 14 publications

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“…Biomarkers for prediction of PE before manifestation of clinical symptoms in early pregnancy would help to identify such cases for more careful follow-up and early interventions[ 4 ]. Currently, there is no definite treatment for PE, except preterm delivery of placenta and fetus, which increases the risk of disability and death of the newborn, especially in severe early-onset cases[ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Accuracy of Soluble Endoglin for Diagnosis of Preeclampsia and its Severity

Nikuei

Rajaei

Malekzadeh

et al. 2017

IBJ

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Background:The use of biomarkers for diagnosis of Preeclampsia (PE), a life-threatening pregnancy disorder, could reduce serious complications of this disease. In this study, we investigated dysregulation of endoglin (Eng) expression and diagnostic accuracy of soluble endoglin (sEng) in PE patients.Methods:For this case-control study, 26 mild and 15 severe preeclamptic women along with 20 normotensive controls were recruited. The expression level of Eng (the co-receptor of TGF-β1) was evaluated using qRT-PCR. Also, the serum concentration of soluble Eng and expression of membranous Eng were determined by ELISA and immunohistochemistry.Results:A significant up-regulation in Eng mRNA and sEng levels was observed in PE patients versus normal controls. Immunohistochemistry (IHC) showed up-regulation of membranous Eng staining in syncytiotrophoblast and cytotrophoblast cells of PE patients. The serum levels of sEng were significantly increased in all patients (mild, sever, early- and late-onset) as compared to healthy pregnant women (P<0.001). Receiver-operating characteristic (ROC) curve analysis revealed that sEng had the highest accuracy in distinguishing PE from normal pregnancies with cut-off value of 20.4, sensitivity of 92.1%, specificity of 90%, and area under the curve (AUC) of 0.94 (95% CI: 0.88-1.00).Conclusions:Our data showed that the up-regulation of Eng mRNA along with its membranous and soluble form in PE patients leads to defect in angiogenesis pathway. Also, the results of this study revealed sEng potential as a marker for diagnosis of PE and its severity.

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Section: Introductionmentioning

confidence: 99%

Accuracy of Soluble Endoglin for Diagnosis of Preeclampsia and its Severity

Nikuei

Rajaei

Malekzadeh

et al. 2017

IBJ

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“…7c and S7i ). Macrophages and dendritic cells showed changes in genes including Osm , involved in invasion under hypoxic conditions (Wie et al, 2018), and transcription factor E2f1 that affects dendritic cell maturation (Fang et al, 2010) and is also implicated in pre-eclampsia (Kaitu’u-Lino et al, 2015). Macrophage cell subsets expressed genes were enriched for dendritic cell maturation, antigen presentation or inflammation genes (FDR = 0.007, 0.02, 0.0001, IPA) ( Table S2 ).…”

Section: Resultsmentioning

confidence: 99%

Parental-fetal interplay of immune genes leads to intrauterine growth restriction

Kaur

Cbm

Ashenberg

et al. 2021

Preprint

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Intrauterine growth restriction (IUGR) of fetuses affects 5-10% of pregnancies and is associated with perinatal morbidity, mortality and long-term health issues. Understanding genetic predisposition to IUGR is challenging, owing to extensive gene polymorphisms, linkage disequilibrium, and maternal and paternal influence. Here, we demonstrate that the inhibitory receptor, KIR2DL1, expressed on maternal uterine natural killer (uNK) cells, in interaction with the paternally-inherited HLA-C*05, an HLA-C group 2 allotype, expressed on fetal trophoblast cells, causes IUGR in a humanised mouse model. Micro-CT imaging of the uteroplacental vasculature revealed reduced uterine spiral artery diameter and increased segment length, increasing fetal blood flow resistance. Single cell RNA-Seq from the maternal-fetal interface highlighted expression programs activated by KIR2DL1-induced IUGR in several placental cell types, including degradation of extracellular matrix components, angiogenesis, and uNK cell communication, suggesting a complex response underlying IUGR. As current IUGR treatments are insufficient, our findings provide important insight for drug development.

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“…A previous study reported that E2F3 expression in FGR placentas was lower than that in the placentas of normal control (18). Another research demonstrated that E2F1 was significantly downregulated in placenta with severe early-onset preeclampsia (19), which is known to be caused by failed EVT invasion. Thus, E2F1 and E2F3 could promote placental growth in human, although their function in human EVTs is not fully known.…”

Section: Discussionmentioning

confidence: 99%

The role of E2F8 in the human placenta

et al. 2018

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Recent studies have reported that E2F transcription factor (E2F) 8, an atypical E2F transcription factor, serves a critical role in promoting the growth and development of the murine placenta. However, the function of E2F8 in the human placenta remains unknown. Invasion of extravillous trophoblasts (EVTs) into the maternal decidua is known to be important for the development of the human placenta. To investigate the role of E2F8 in human placental development, E2F8 localisation was examined in the human placenta and E2F8 mRNA expression was detected in primary cultured EVTs. The human EVT cell line, HTR-8/SVneo, was divided into two groups and treated separately, one with retrovirus expressing short hairpin (sh)-RNA against E2F8 (shE2F8 cells) and the other with non-target control shRNA (shControl cells). The cell functions, including cell cycle, proliferation, invasion and adhesion, were compared between the shE2F8 and shControl cells. A histological examination revealed that E2F8 was localised in the decidua cells, EVTs, and cytotrophoblasts in the placenta. E2F8 mRNA was confirmed to be expressed in cultured primary EVTs. No significant difference was observed in the cell cycle, proliferation or adhesion between the shE2F8 and shControl cells. The invasive ability was ~2-fold higher in the shE2F8 cells when compared with the shControl cells (P<0.01). Production of matrix metalloproteinase-1 was significantly increased in the shE2F8 cells when compared with the shControl cells (P<0.05). Taken together, E2F8 is present in the EVTs of the human placenta, but, unlike murine placenta, it may suppress the invasiveness of EVTs. E2F8 was also present in cytotrophoblasts in cell columns, which have no invasive ability and differentiate into EVTs. In conclusion, E2F8 also exists in the human placenta, and its function may be different from that in the murine placenta, although further investigation is required.

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Transcription factors E2F1 and E2F3 are expressed in placenta but do not regulate MMP14

Cited by 9 publications

References 14 publications

Accuracy of Soluble Endoglin for Diagnosis of Preeclampsia and its Severity

Accuracy of Soluble Endoglin for Diagnosis of Preeclampsia and its Severity

Parental-fetal interplay of immune genes leads to intrauterine growth restriction

The role of E2F8 in the human placenta

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