Expression of proliferation and apoptotic markers in human placenta during pregnancy

Danihel, Ľ; Gomolcák, P; Korbeľ, M; Pruzinec, Jozef; Vojtassák, J; Janík, Peter; Babál, Pavel

doi:10.1078/0065-1281-00683

Cited by 34 publications

(16 citation statements)

References 10 publications

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“…This finding is consistent with other studies, which have shown that proliferation of placental cells decreases throughout gestation [61][62][63]. Following injection of TNP-470, the number of proliferating ECs at E13.5 and E18.5 decreased significantly (by about 40%) in comparison with the control group.…”

Section: Discussionsupporting

confidence: 95%

Induction of Intrauterine Growth Restriction by Reducing Placental Vascular Growth with the Angioinhibin TNP-470

Mukhopadhyay¹,

Underwood²,

Clyde³

et al. 2005

Biology of Reproduction

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The placenta is a specialized vascular interface between the maternal and fetal circulations that increases in size to accommodate the nutritional and metabolic demands of the growing fetus. Vascular proliferation and expansion are critical components of placental development and, consequently, interference with vascular growth has the potential to severely restrict concurrent development of both the placenta and fetus. In this study, we describe the effects of an antiangiogenic agent, TNP-470, on placental vascular development and the induction of a form of intrauterine growth restriction (IUGR) in mice. Administration of TNP-470 to dams in the second half of pregnancy resulted in a smaller maternal weight gain accompanied by decreased placental and fetal sizes in comparison with control animals. Total numbers of fetuses per litter were not affected significantly. Stereological analysis of placentas revealed no changes in the combined lengths of vessels. However, the mean cross-sectional areas of maternal and fetal vessels in the labyrinth of TNP-470-treated mice were reduced at Embryonic Day 13.5 (E13.5) but not at E18.5. Further analysis showed reduced placental endothelial proliferation at E13.5 and E18.5 in TNP-470-treated animals. No other structural or morphometric differences in placentas were detected between TNP-470-treated and control mice at E18.5. This study provides conclusive evidence that administration of TNP-470 interferes with placental vascular proliferation and vessel caliber and results in a reproducible model of IUGR.

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Section: Discussionsupporting

confidence: 95%

Induction of Intrauterine Growth Restriction by Reducing Placental Vascular Growth with the Angioinhibin TNP-470

Mukhopadhyay¹,

Underwood²,

Clyde³

et al. 2005

Biology of Reproduction

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“…Our ratio of 1:3, cytotrophoblast to syncytiotrophoblast at 9 weeks gestation, indicates a predominance of cytotrophoblasts at this time, but also alludes to a reduction in their relative numbers in late pregnancy, not solely due to spatial dispersal. Although contrary to the findings of Simpson et al (1992), this conclusion is in accordance with a number of past studies showing a decline through gestation in the frequency of cytotrophoblast mitosis and incidence of proliferation nuclear markers such as PCNA (proliferating cell nuclear antigen) and Ki-67 (Chan et al 1999;Danihel et al 2002;Muhlhauser et al 1993;Watanabe et al 1993). …”

Section: Discussionsupporting

confidence: 51%

E-cadherin in the assessment of aberrant placental cytotrophoblast turnover in pregnancies complicated by pre-eclampsia

Brown

Lacey

Baker

et al. 2005

Histochem Cell Biol

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E-cadherin is a cell-cell adhesion protein expressed in cytotrophoblasts, which is lost as they differentiate and syncytialise. We have exploited E-cadherin as a marker of cytotrophoblasts to investigate villous tissue composition in first and third trimester placentae, both in normal pregnancy and pregnancies complicated by pre-eclampsia. We have achieved this by measuring expression levels of E-cadherin at the mRNA level, using Q-PCR, and at the protein level using semi-quantitative Western blotting. We have also combined E-cadherin immunohistochemistry with morphometric analysis of area measurements to define cytotrophoblast and syncytiotrophoblast compartments. This novel use of E-cadherin has revealed a decrease in the proportion of cytotrophoblasts in villous tissue as pregnancy progresses, in the absence of changes in syncytiotrophoblast cover. Moreover, in pre-eclampsia, placental E-cadherin was raised compared to syncytiotrophoblast, suggesting either exaggerated cytotrophoblast proliferation or impaired cytotrophoblast differentiation, both alterations of potential pathogenic importance.

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“…Proliferation is mostly confined to the CTB progenitor cell layer and is a vital process in the formation of anchoring columns in early gestation that attach the placenta to the uterine wall. Interestingly, proliferative markers decline later in gestation coinciding with a reduction in placental growth [51]. On the other hand, proliferative markers in the STB layer are not detected at any stage of pregnancy.…”

Section: Key Processes In Human Placental Developmentmentioning

confidence: 99%

MicroRNAs in Human Placental Development and Pregnancy Complications

Brkić

Hayder

et al. 2013

IJMS

222

167

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MicroRNAs (miRNAs) are small non-coding RNAs, which function as critical posttranscriptional regulators of gene expression by promoting mRNA degradation and translational inhibition. Placenta expresses many ubiquitous as well as specific miRNAs. These miRNAs regulate trophoblast cell differentiation, proliferation, apoptosis, invasion/migration, and angiogenesis, suggesting that miRNAs play important roles during placental development. Aberrant miRNAs expression has been linked to pregnancy complications, such as preeclampsia. Recent research of placental miRNAs focuses on identifying placental miRNA species, examining differential expression of miRNAs between placentas from normal and compromised pregnancies, and uncovering the function of miRNAs in the placenta. More studies are required to further understand the functional significance of miRNAs in placental development and to explore the possibility of using miRNAs as biomarkers and therapeutic targets for pregnancy-related disorders. In this paper, we reviewed the current knowledge about the expression and function of miRNAs in placental development, and propose future directions for miRNA studies.

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Expression of proliferation and apoptotic markers in human placenta during pregnancy

Cited by 34 publications

References 10 publications

Induction of Intrauterine Growth Restriction by Reducing Placental Vascular Growth with the Angioinhibin TNP-470

Induction of Intrauterine Growth Restriction by Reducing Placental Vascular Growth with the Angioinhibin TNP-470

E-cadherin in the assessment of aberrant placental cytotrophoblast turnover in pregnancies complicated by pre-eclampsia

MicroRNAs in Human Placental Development and Pregnancy Complications

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