CD97 Is Decreased in Preeclamptic Placentas and Promotes Human Trophoblast Invasion Through PI3K/Akt/mTOR Signaling Pathway

Shen, Huaxiang; Jin, Mingzhu; Gu, Shengyi; Wu, Yong; Yang, Mengnan; Hua, Xiaolin

doi:10.1177/1933719119828067

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…In gastric cancer and oral squamous cancer tissues, T-cadherin suppresses cell proliferation and invasion via the overexpressing AKT/mTOR signalling pathway (41,42). In placental tissue, suppression of the PI3K/Akt/mTOR signalling pathway was shown to cause the development of preeclampsia by decreasing trophoblast invasion (43)(44)(45). A recent study reported that, decreasing CD97 expression in placenta could downregulate PI3K/Akt/mTOR signaling pathway via Forkhead box protein C2 (FOXC2), leading to decreased trophoblast invasion, which contributes to the development of preeclampsia in late pregnancy (43).…”

Section: Biyik Et Almentioning

confidence: 99%

“…In placental tissue, suppression of the PI3K/Akt/mTOR signalling pathway was shown to cause the development of preeclampsia by decreasing trophoblast invasion (43)(44)(45). A recent study reported that, decreasing CD97 expression in placenta could downregulate PI3K/Akt/mTOR signaling pathway via Forkhead box protein C2 (FOXC2), leading to decreased trophoblast invasion, which contributes to the development of preeclampsia in late pregnancy (43). In this study, the fact that T-cadherin is increased when trophoblast invasion is reduced shows that it suppresses trophoblast invasion.…”

Section: Biyik Et Almentioning

confidence: 99%

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Placental T-Cadherin Correlates With Trophoblastic Invasion Anomalies: Placenta Percreta and Fetal Growth Restriction

Bıyık

Metineren

Öztürk

et al. 2022

International Journal of Gynecological Pathology

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In this study, we compared the placental T-cadherin staining intensity of pregnant women with placenta percreta (PP) and asymmetrical fetal growth restriction (FGR) compared with healthy control pregnancies. Placental T-cadherin levels of the placenta of 86 pregnant women in total, 25 with FGR, 30 with healthy pregnant subjects, and 31 with PP, were examined using monoclonal anti-T-cadherin (CDH13) antibody for immunohistochemical examination. In immunohistochemistry, H-scores were used for each group to compare the expression of T-cadherin in extravillous trophoblast (EVT) cells. T-cadherin H-score of EVTs was highest in the FGR group and the lowest in the PP group. The difference in H-score between the FGR group and the control group was not statistically significant (P = 0.344). The difference between the PP group and the other 2 groups was significant (Po0.0001). Multivariable linear regression analysis with a stepwise elimination method was performed in order to identify demographic and clinical parameters with significant effects on the T-cadherin H-score of EVTs. The estimation results identified only the disease group as a significant predictor of the H-score of EVTs (R 2 = 0.340, Po0.0001). The highest T-cadherin H-score of EVTs was found in the FGR group and the lowest in the PP group. The low T-cadherin H-score values in the PP group suggest that low T-cadherin EVTs may be associated with increased placental invasion. Likewise, despite the statistical insignificance, a higher T-cadherin H-score of EVTs in FGR compared with controls implies a decreased invasiveness of the placenta in FGR.

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Section: Biyik Et Almentioning

confidence: 99%

Section: Biyik Et Almentioning

confidence: 99%

Placental T-Cadherin Correlates With Trophoblastic Invasion Anomalies: Placenta Percreta and Fetal Growth Restriction

Bıyık

Metineren

Öztürk

et al. 2022

International Journal of Gynecological Pathology

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CD97 expression level and its effect on cell adhesion in Preeclampsia

Atıgan

Tan

Çetin

et al. 2022

BMC Pregnancy Childbirth

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Objectives Cellular interactions and cell adhesion underlie preeclampsia (PE). The aim of the current study is to investigate the role of cell adhesion molecules such as CD97, neural (N)-cadherin, epithelial (E) -cadherin and integrin beta-4 in PE. Methods This prospective study included 20 pregnant women with PE and a control group of 16 healthy pregnant women who were matched for age, gestational age, gravida and parity. Standard blood tests and placental cell adhesion molecule immunohistochemical staining were examined. Results The creatinine, uric acid and lactate dehydrogenase (LDH) levels from standard blood tests were found to be statistically higher in the PE group (p = 0.002, p = 0.000, p = 0.001; respectively). In the PE group, the CD97 maternal serum level was statistically significantly lower, as was its immunohistochemical expression in placental sections (p = 0.028, p = 0.000; respectively). The E-cadherin expression score was statistically higher in the PE group compared to the control group (3,65 ± 1,84 vs 2,06 ± 1,76 respectively; p = 0.003). The N-cadherin expression score was statistically lower in the PE group compared to the control group (1,50 ± 0,82 vs 2,43 ± 1,59 respectively; p = 0.049). Integrin beta-4 was not statistically different between groups. Conclusions Cellular interaction may be responsible for PE as in cancer. A balance in intercellular communication, as researched in cancer therapy, may offer the solution in PE.

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Focusing on the role of secretin/adhesion (Class B) G protein-coupled receptors in placental development and preeclampsia

Yin

Guan

Zhang

et al. 2022

Front. Cell Dev. Biol.

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Preeclampsia, a clinical syndrome mainly characterized by hypertension and proteinuria, with a worldwide incidence of 3–8% and high maternal mortality, is a risk factor highly associated with maternal and offspring cardiovascular disease. However, the etiology and pathogenesis of preeclampsia are complicated and have not been fully elucidated. Obesity, immunological diseases and endocrine metabolic diseases are high-risk factors for the development of preeclampsia. Effective methods to treat preeclampsia are lacking, and termination of pregnancy remains the only curative treatment for preeclampsia. The pathogenesis of preeclampsia include poor placentation, uteroplacental malperfusion, oxidative stress, endoplasmic reticulum stress, dysregulated immune tolerance, vascular inflammation and endothelial cell dysfunction. The notion that placenta is the core factor in the pathogenesis of preeclampsia is still prevailing. G protein-coupled receptors, the largest family of membrane proteins in eukaryotes and the largest drug target family to date, exhibit diversity in structure and function. Among them, the secretin/adhesion (Class B) G protein-coupled receptors are essential drug targets for human diseases, such as endocrine diseases and cardiometabolic diseases. Given the great value of the secretin/adhesion (Class B) G protein-coupled receptors in the regulation of cardiovascular system function and the drug target exploration, we summarize the role of these receptors in placental development and preeclampsia, and outlined the relevant pathological mechanisms, thereby providing potential drug targets for preeclampsia treatment.

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CD97 Is Decreased in Preeclamptic Placentas and Promotes Human Trophoblast Invasion Through PI3K/Akt/mTOR Signaling Pathway

Cited by 4 publications

References 27 publications

Placental T-Cadherin Correlates With Trophoblastic Invasion Anomalies: Placenta Percreta and Fetal Growth Restriction

Placental T-Cadherin Correlates With Trophoblastic Invasion Anomalies: Placenta Percreta and Fetal Growth Restriction

CD97 expression level and its effect on cell adhesion in Preeclampsia

Focusing on the role of secretin/adhesion (Class B) G protein-coupled receptors in placental development and preeclampsia

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