Immunolocalization of PCNA, Ki67, p27 and p57 in normal and dexamethasone-induced intrauterine growth restriction placental development in rat

Unek, Gozde; Ozmen, Asli; Kipmen-Korgun, Dijle; Korgun, Emin Türkay

doi:10.1016/j.acthis.2011.02.002

Cited by 24 publications

(23 citation statements)

References 36 publications

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“…Moreover, after day 17, scarcely any Ki67 immunostaining was obtained in the IUGR placentas in the junctional zone. 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].…”

Section: The Effects Of Glucocorticoids On Placental Cell Cyclesupporting

confidence: 73%

“…We observed that p57 immunostaining intensities in Dex-induced IUGR placentas were stronger compared to controls in both zones for all gestational days. 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].…”

Section: The Effects Of Glucocorticoids On Placental Cell Cyclecontrasting

confidence: 56%

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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 Cyclesupporting

confidence: 73%

Section: The Effects Of Glucocorticoids On Placental Cell Cyclecontrasting

confidence: 56%

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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“…Trophoblast proliferation being necessary for normal placental development shows a decrease as a result of some pathological cases. Unek [46] stated that PCNA positivity decreased significantly as compared with the control group in the placentas of rats where IUGR was formed. In the study performed by Acar [25] PCNA immunopositive cell frequency was reported to decrease in the control group and diabetic rat placentas in parallel with gestation age but this positivity was reported to increase more as a result of diabetes.…”

Section: Discussionmentioning

confidence: 97%

“…In a previous study [46], TUNEL-positive cells found in fetal and maternal part of the placenta were counted on gestation day 20 and the number of apoptotic cells in the maternal part was reported to be higher than the ones in the fetal part. In another study [54], apoptotic cells in rat placenta on gestation day 18 were reported to rarely exist.…”

Section: Discussionmentioning

confidence: 99%

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

Erboğa

Kanter

2015

Biol Trace Elem Res

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In this study, we aimed to show how cadmium (Cd) affects the trophoblast proliferation and differentiation in the placenta and the apoptotic activity in different gestational days and, hence, its effects of placental development with immunohistochemical and TUNEL techniques. Experimental model of our study consisted of placental development of control and Cd groups on 15, 17, 19, and 21th days of the gestation. Female rats in Cd groups were subcutaneously administered a single dose of 0.5 mg Cd/kg/day dissolved in sodium chloride as 2 mL/kg Cd chloride until the day they sacrificed. Embryo and placenta of female rats were separately removed on 15, 17, 19, and 21th days of the gestation in which the placental development takes place and placentas were processed for microscopic examinations. In the placentas of the control group, all layers were observed to be formed on the 15th gestational day and thereafter a continuous growth was monitored. In the Cd group also all layers existed from the 15th gestational day. However, they were smaller in size than control groups. Frequency of proliferating cell nuclear antigen (PCNA)-positive cells was decreased and the number of apoptotic cells was increased in all the gestational days related to Cd. In conclusion, Cd administered during the pregnancy was observed to cause abnormal placental development by disrupting the normal structure of the placenta, inhibiting the proliferation of trophoblast and increasing the number of apoptotic trophoblast cells.

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“…One of the reasons for IUGR is abnormal placentation. Overexposure to glucocorticoids causes IUGR in animal models (Seckl 1994;Gluckman 2001;Unek et al 2011). In rats, fetal-placental exposure to maternally administered glucocorticoids decreases birth weight and placental weight (Benediktsson et al 1993;Sugden et al 2001;McDonald et al 2003).…”

Section: Introductionmentioning

confidence: 99%

The expression of Akt and ERK1/2 proteins decreased in dexamethasone-induced intrauterine growth restricted rat placental development

et al. 2011

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The placenta is a complicated tissue that lies between maternal and fetal compartments. Although the architecture of the human and rodent placentas differ a little in their details, their overall structures and the molecular mechanisms of placental developments are thought to be very similar. In rats, fetal-placental exposure to maternally administered glucocorticoids decreases birth weight and placental weight. The mechanism underlying the placental growth inhibitory effects of glucocorticoids have not been elucidated. Moreover it is still not determined that how Akt and ERK1/2 proteins related proliferation and apoptosis mechanisms are influenced by dexamethasone-induced IUGR (Intrauterine Growth Restriction) placentas. The aim of this study was to investigate the expression levels and spatio-temporal immunolocalizations of Akt, p-Akt, ERK1/2 and p-ERK1/2 proteins in normal and dexamethasone treated placental development in pregnant Wistar rats. Pregnant rats were subcutaneously injected with 100 μg/kg dexamethasone 21-acetate in 0.1 ml 10% ethanol on day 10 and 12 of gestation. Afterwards injection was continued as 200 μg/kg until they were killed on day 12 (injection started on day 10), 14, 16, 18 and 20 (injections started on day 12) of pregnancy. Placental and embryonal tissues were collected for immunohistochemistry and Western blot analysis. We found that maternal dexamethasone treatment led to a decrease in ERK1/2 and Akt activation during rat placental development. The decrease in Akt and ERK1/2 activations may result with cell survival inhibition or apoptosis stimulation. Hence, dexamethasone induced placental and embryonal developmental abnormalities could be associated with reduction of Akt and ERK1/2 activation.

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Immunolocalization of PCNA, Ki67, p27 and p57 in normal and dexamethasone-induced intrauterine growth restriction placental development in rat

Cited by 24 publications

References 36 publications

The Effects of Glucocorticoids on Fetal and Placental Development

The Effects of Glucocorticoids on Fetal and Placental Development

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

The expression of Akt and ERK1/2 proteins decreased in dexamethasone-induced intrauterine growth restricted rat placental development

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