The expression of Cdk inhibitors p27kip1 and p57kip2 in mouse placenta and human choriocarcinoma JEG-3 cells

Kim, S.T.; Lee, S.K.; Gye, Myung Chan

doi:10.1016/j.placenta.2004.04.008

Cited by 16 publications

(14 citation statements)

References 18 publications

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“…We found that Dex-induction results in p57 upregulation in rat placental development [89]. In contrast to our results, p57 was not expressed in Dex-induced JEG-3 cells [90]. In another study, we wanted to determine the Ser/Thr protein kinase Akt and a MAPK (Mitogen-Activated Protein Kinase) ERK1/2 related proliferation and apoptosis mechanisms are influenced by Dex-induced IUGR placentas.…”

Section: The Effects Of Glucocorticoids On Placental Cell Cyclecontrasting

confidence: 85%

“…We found stronger p27 immunolabeling intensity in Dex-induced IUGR placentas when compared to control placentas in both junctional and labyrinth zones for all gestational days (Table 1) [89]. In accordance with this, in another study, it was observed that in the Dex-induced human choriocarcinoma JEG-3 cells p27 mRNAs were upregulated [90]. We observed that p57 immunostaining intensities in Dex-induced IUGR placentas were stronger compared to controls in both zones for all gestational days.…”

Section: The Effects Of Glucocorticoids On Placental Cell Cyclesupporting

confidence: 85%

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The Effects of Glucocorticoids on Fetal and Placental Development

Korgun¹,

Ozmen²,

Unek³

et al. 2012

Glucocorticoids - New Recognition of Our Familiar Friend

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Section: The Effects Of Glucocorticoids On Placental Cell Cyclecontrasting

confidence: 85%

Section: The Effects Of Glucocorticoids On Placental Cell Cyclesupporting

confidence: 85%

The Effects of Glucocorticoids on Fetal and Placental Development

Korgun¹,

Ozmen²,

Unek³

et al. 2012

Glucocorticoids - New Recognition of Our Familiar Friend

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“…The Cdkn1c gene is expressed at much lower levels at E10.5, a stage when other Cip/Kip family members exhibit higher expression (Kim et al 2005). An assay to test the predicted increase in bw × po placental Cdkn1c expression was again suggestive of that trend, but the differences were not significant.…”

Section: Perturbation Of Cell Cycle Regulatory Genes In the F 1 Hybridsmentioning

confidence: 99%

“…The latter condition is characterised by an overgrowth of trophoblast (placental) tissue and lack of a fetus. Other imprinted genes in this region, such as Cdkn1c/p57 kip2 (a cyclin-dependent kinase inhibitor), show similar associations (Takahashi et al 2000;Kim et al 2005). Such perturbations are typically accompanied by altered patterns of one or more epigenetic marks (e.g.…”

Section: Introductionmentioning

confidence: 99%

Changes in cell cycle and extracellular matrix gene expression during placental development in deer mouse (Peromyscus) hybrids

Duselis

Obergfell

Mack

et al. 2007

Reprod. Fertil. Dev.

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Abstract.Crosses between two species of the rodent genus Peromyscus produce defects in both growth and development. The defects are pronounced in the hybrid placentas. Peromyscuys maniculatus (strain BW) females mated to P. polionotus (strain PO) males produce placentas half the size of the parental species, as well as growth-retarded embryos. In contrast, PO females mated to BW males result in defective conceptuses that display embryonic and placental overgrowth. These 'parent-of-origin'-dependent phenotypes are consistent with previous studies that demonstrated altered expression of imprinted genes and genetic linkage of the overgrowth phenotypes to imprinted domains. In the present study, we take a broader approach in assessing perturbations in hybrid placental gene expression through the use of Mus musculus cDNA microarrays. In verifying classes of genes identified in microarray screens differentially regulated during hybrid placental development, we focused on those influencing the cell cycle and extracellular matrix (ECM). Our work suggests that cell cycle regulators at the G 1 /S phase check-point are downregulated in the large hybrid placenta, whereas the small hybrid placenta is more variable. The ECM genes are typically downstream targets of cell cycle regulation and their misregulation is consistent with many of the dysmorphic phenotypes. Thus, these data suggest imbalances in proliferation and differentiation in hybrid placentation.

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“…There are only a limited number of studies reporting the presence of p21, p27 and p57 in human and rodent placenta (McKenzie et al 1998;Zhang et al 1998;Bamberger et al 1999;Genbacev et al 2000;Takahashi et al 2000;Olvera et al 2001;Yamauchi et al 2004;Kim et al 2005;Korgun et al 2006;Gundogan et al 2010). Analysis of p57-deficient mice showed that placentomegaly was associated with an increase in labyrinthine cytotrophoblasts and spongiotrophoblast cell numbers, but the underlying mechanisms could not be explained (Takahashi et al 2000).…”

Section: Cip/kip Cell Cycle Inhibitorsmentioning

confidence: 99%

Mapping of CIP/KIP inhibitors, G1 cyclins D1, D3, E and p53 proteins in the rat term placenta

Korgun

Unek

Herrera

et al. 2011

Histochem Cell Biol

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As cell cycle regulation is fundamental to the normal growth and development of the placenta, the aim of the present study was to determine the immunolocalizations of cell cycle related proteins, which have key roles in proliferation, differentiation and apoptosis during the development of the rat placenta. Here immunohistochemistry has been used to localize G1 cyclins (D1, D3, E), which are major determinants of proliferation, CIP/KIP inhibitors (p21, p27, p57), p53 as a master regulator and proliferating cell nuclear antigen in all cell types of the rat term placenta. The proportion of each cell type immunolabeled was counted. Cyclin D1 and cyclin D3 were present mostly in cells of the fetal aspect of the placenta, whereas the G1/S cyclin E was present only in the spongio- and labyrinthine trophoblast populations. Among the CIP/KIP inhibitors, p21 was present only in cells of the fetal aspect whereas p27 and p57 were found in all cell types studied. p53 was only found in a small proportion of cells with no co-localization of p53 and p21. The data suggest that the cells of the fetal side of the rat placenta still have some proliferation potential which is kept in check by expression of the CIP/KIP cell cycle inhibitors, whereas cells of the maternal aspect have lost this potential. Apoptosis is only marginal in the term rat placenta. In conclusion, proliferation and apoptosis in rat placental cells appears controlled mostly by the CIP/KIP inhibitors in late pregnancy.

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The expression of Cdk inhibitors p27kip1 and p57kip2 in mouse placenta and human choriocarcinoma JEG-3 cells

Cited by 16 publications

References 18 publications

The Effects of Glucocorticoids on Fetal and Placental Development

The Effects of Glucocorticoids on Fetal and Placental Development

Changes in cell cycle and extracellular matrix gene expression during placental development in deer mouse (Peromyscus) hybrids

Mapping of CIP/KIP inhibitors, G1 cyclins D1, D3, E and p53 proteins in the rat term placenta

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