The expression of cell cycle related proteins PCNA, Ki67, p27 and p57 in normal and preeclamptic human placentas

Unek, Gozde; Ozmen, Asli; Mendilcioğlu, İnanç; Şi̇mşek, Mehmet; Korgun, Emin Türkay

doi:10.1016/j.tice.2014.04.003

Cited by 32 publications

(22 citation statements)

References 42 publications

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“…A, Schematic representation of GR binding sites either overlapping or in close proximity to the chromosomal location of SERPINE1. 69 In addition to reducing cell migration and proliferation, glucocorticoids also reduced invasion in Sw.71 cells. B-D, ChIP assays were performed against IgG, GR, or PolII in cells treated with vehicle (Veh) or 100 nmol/L Dex.…”

Section: Discussionmentioning

confidence: 97%

“…68 One recent study demonstrated decreased rates of proliferation of EVTs for women with preeclampsia. 69 In addition to reducing cell migration and proliferation, glucocorticoids also reduced invasion in Sw.71 cells. Shallow trophoblast invasion has detrimental consequences on placentation and has been implicated in a number of pregnancy complications such as preeclampsia and intra-uterine growth restriction (IUGR).…”

Section: Discussionmentioning

confidence: 97%

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Glucocorticoid signaling regulates cell invasion and migration in the human first‐trimester trophoblast cell line Sw.71

Kisanga

Tang

Guller

et al. 2018

American J Rep Immunol

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 97%

Glucocorticoid signaling regulates cell invasion and migration in the human first‐trimester trophoblast cell line Sw.71

Kisanga

Tang

Guller

et al. 2018

American J Rep Immunol

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“…For example, the maternally expressed imprinted gene CYCLIN-DEPENDENT KINASE INHIBITOR 1C ( CDKN1C ) has variously been reported to be significantly decreased [97], increased [98, 99], or unaltered [100] in preeclamptic placentas. These conflicting results may be explained by a difference in mode of delivery, given recent evidence demonstrating significantly increased CDKN1C expression in laboring versus non-laboring placentas [101].…”

Section: Methodsmentioning

confidence: 99%

Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes

Nomura

Roshan

Janssen

et al. 2017

Arch Gynecol Obstet

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Purpose Preeclampsia is known to be a leading cause of mortality and morbidity among mothers and their infants. Approximately 3–8% of all pregnancies in the US are complicated by preeclampsia and another 5–7% by hypertensive symptoms. However, less is known about its long-term influence on infant neurobehavioral development. The current review attempts to demonstrate new evidence for imprinting gene dysregulation caused by hypertension, which may explain the link between maternal preeclampsia and neurocognitive dysregulation in offspring. Method Pub Med and Web of Science databases were searched using the terms “preeclampsia,” “gestational hypertension,” “imprinting genes,” “imprinting dysregulation,” and “epigenetic modification,” in order to review the evidence demonstrating associations between preeclampsia and suboptimal child neurodevelopment, and suggest dysregulation of placental genomic imprinting as a potential underlying mechanism. Results The high mortality and morbidity among mothers and fetuses due to preeclampsia is well known, but there is little research on the long-term biological consequences of preeclampsia and resulting hypoxia on the fetal/child neurodevelopment. In the past decade, accumulating evidence from studies that transcend disciplinary boundaries have begun to show that imprinted genes expressed in the placenta might hold clues for a link between preeclampsia and impaired cognitive neurodevelopment. A sudden onset of maternal hypertension detected by the placenta may result in misguided biological programming of the fetus via changes in the epigenome, resulting in suboptimal infant development. Conclusion Furthering our understanding of the molecular and cellular mechanisms through which neurodevelopmental trajectories of the fetus/infant are affected by preeclampsia and hypertension will represent an important first step toward preventing adverse neurodevelopment in infants.

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“…Given E2F1 is touted as a cell cycle activator, its decreased expression in PE may possibly be reflective of a failing placenta. Certainly a recent study suggesting enhanced expression of cell cycle inhibitors p27 and p57 within PE placentas compared to control would support the notion that cells within the PE placenta are in a state of cell cycle repression rather than activation [15].…”

Section: Discussionmentioning

confidence: 93%

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

et al. 2015

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The expression of cell cycle related proteins PCNA, Ki67, p27 and p57 in normal and preeclamptic human placentas

Cited by 32 publications

References 42 publications

Glucocorticoid signaling regulates cell invasion and migration in the human first‐trimester trophoblast cell line Sw.71

Glucocorticoid signaling regulates cell invasion and migration in the human first‐trimester trophoblast cell line Sw.71

Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes

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

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