8 research outputs found
Cell cycle inhibitor p57 expression in normal and diabetic rat placentas during some stages of pregnancy
Placentomegaly, an abnormal increase in the size of the placenta, is commonly seen in human diabetic pregnancies and diabetic animal experimental models. Proper placental development depends on the proliferation and differentiation of trophoblasts. However, our knowledge about the mitotic regulators that play key roles in synchronizing these events is limited. p57 is a cyclin-dependent kinase (CDK) inhibitor acting in the G1/S transition of the cell cycle. There is no data regarding p57 expression in either rat or human diabetic placentas. The purpose of this study was to investigate p57 expression in control and diabetic rat placentas at different stages of pregnancy. Diabetes was induced by streptozotocin on the first day of pregnancy, and placentas were taken on days 11, 13, 17, and 21 of pregnancy. Our results showed that on day 11, p57 immunostaining intensity was stronger in control group placentas compared to the diabetic group. On day 13, p57 immunostaining intensity increased in both groups, but increased more in the diabetic group. On day 17, p57 immunostaining intensity decreased in both the control and diabetic groups compared to day 13, yet the intensity remained higher in control placentas compared to diabetic placentas. On day 21 of pregnancy, p57 immunostaining intensity increased in the control group and it decreased from the day 17 level in the diabetic group. Western blot results showed consistency with immunohistochemistry results. Our study shows different expression patterns of p57 between control and diabetic rat placentas, which indicate p57 may play a role in abnormal placental formation resulting in placentomegaly arising from diabete
The PI3K/Akt and MAPK-ERK1/2 pathways are altered in STZ induced diabetic rat placentas
Diabetic pregnancy is associated with
complications such as early and late embryonic death,
fetal growth disorders, placental abnormalities, and
embryonal-placental metabolic disorders. Excessive
apoptosis and/or changes of proliferation mechanisms
are seen as a major event in the pathogenesis of diabetesinduced
embryonic death, placental weight and
structural anomalies.
Akt and ERK1/2 proteins are important for placental
and fetal development associated with cellular
proliferation and differentiation mechanisms. The
mechanism underlying the placental growth regulatory
effects of hyperglycemia have not been elucidated.
Moreover, it is still not determined how Akt and ERK1/2
proteins related proliferation and apoptosis mechanisms
are influenced by Streptozotocin (STZ) induced diabetic
rat placental development.
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 STZ-treated diabetic rat placental
development. In order to compose the diabetic group,
pregnant females were injected with a single dose of
40mg/kg STZ intraperitonally seven days before their
sacrifice at 12th, 14th, 16th, 18th and 20th day of their
gestation.
We found that maternal diabetic environment led to
a decrease in ERK1/2 and Akt phosphorylation during
rat placental development. It could be said that MAPK ERK1/2 and PI3K/Akt cell signaling pathways are
affected from hyperglycemic conditions in rat placentas.
In conclusion, hyperglycemia-induced placental and
embryonal developmental abnormalities could be
associated with reduction of Akt and ERK1/2
phosphorylation
The proliferation mechanism of normal and pathological human placentas
The placenta, which is a regulator organ for
many metabolic activities between mother and fetus, is
critical in influencing the outcome of pregnancy.
Therefore, fetal growth is directly related to the placental
development. Placental development depends on the
coordinated action of trophoblast proliferation,
differentiation and invasion. Studies on cell cycle related
proteins that control these events are limited. Abnormal
placental development is linked to various pregnancy
pathologies such as preeclampsia, intrauterine growth
restriction, diabetes mellitus and gestational
trophoblastic diseases. The cell cycle mechanism of
human placenta should be well understood for a healthy
pregnancy outcome. Moreover, how cell cycle related
proteins that control placental development are affected
in pregnancy pathologies is not fully understood yet.
Therefore, the aim of this review is to address the
currently available knowledge on cell cycle regulatory
proteins involved in human placental development and
on the expression differences of these proteins in
pathological placentas