Increased levels of DNA methyltransferases in the placentas of women affected by Placenta Accreta Spectrum lead to aberrant DNA methylation patterns.

Placenta Accreta Spectrum (PAS) is a serious placental abnormality assosiated with significant maternal death during pregnancy. Due to its invasive characteristics resembling tumor growth, PAS is often associated with tumor-related proteins. While DNA methylation is known to regulate genes involved in development, its potential role in the development of PAS remains unclear.

The immunomodulator effect of Bertoni mediated by TNF-α and IL-1β in peripheral blood in diabetic rats.

Bertoni, which is a medicinal plant used in the treatment of diabetes, was the focus of this study aiming to investigate its immunomodulatory properties in diabetes. To form the diabetes group, rats were injected intraperitoneally with STZ and rats with blood glucose levels above 200 mg/dL 2 days after STZ injection were included in the diabetes group. To form the stevia and diabetes + stevia groups, stevia was administered daily by gavage to both healthy and diabetic rats for 28 days.

Effects of Hyperglycemia on Angiogenesis in Human Placental Endothelial Cells.

The placenta is a temporary organ that provides communication between the mother and fetus. Maternal diabetes and abnormal placental angiogenesis may be linked. We investigated the angiogenesis mechanism resulting from VEGF and glucose stimulation in PECs obtained from human term placenta.

Are innate lymphoid cells friend or foe in human pregnancy?

Innate lymphoid cells (ILCs) are involved in the innate immune system because they lack specific antigen receptors and lineage markers. ILCs also display phenotypic and characteristic features of adaptive immune cells. Therefore, ILCs are functional in essential interactions between adaptive and innate immunity.

Effects of Stevioside on the Expressions of GLUT 1, GLUT 3, and GLUT 4 Proteins in Diabetic Rat Placenta.

The placenta provides maternal-fetal nutrient transport. The primary source of energy for fetus development is glucose and maternal-fetal glucose transport occurs through glucose transporters (GLUTs). Stevioside, a component of Bertoni, is used for medicinal and commercial purposes.

Contribution of Human Trophoblast Progenitor Cells to Neurogenesis in Rat Focal Cerebral Ischemia Model.

Objective: : A decrease in the blood flow below a current level in the brain results in ischemia. Studies demonstrated that human trophoblast progenitor cells (hTPCs) contribute to the treatment of many diseases. Therefore, hTPCs might be a promising source to repair ischemia in cerebral ischemia models.

Effects of amnion derived mesenchymal stem cells on fibrosis in a 5/6 nephrectomy model in rats.

Chronic kidney disease (CKD) is characterized by disruption of the glomerulus, tubule and vascular structures by renal fibrosis. Mesenchymal stem cells (MSC) ameliorate CKD. We investigated the effects of human amnion derived MSC (hAMSC) on fibrosis using expression of transforming growth factor beta (TGF-β), collagen type I (COL-1) and bone morphogenetic protein (BMP-7).

Human placental trophoblast progenitor cells (hTPCs) promote angiogenesis and neurogenesis after focal cerebral ischemia in rats.

Introduction: Reduction of blood flow below a threshold value in brain regions locally or globally is called cerebral ischemia and proper treatment requires either the restoration of normal blood flow and/or the administration of neuroprotective therapies. Human trophoblast progenitor cells (hTPCs) give rise to the placenta and are responsible for the invasion and vascular remodeling of the maternal vessels within the uterus. Here, we tested whether hTPCs promoted to differentiate along neural lineages may exhibit therapeutic properties in the setting of cerebral ischemia .

Effects of Human Placental Amnion Derived Mesenchymal Stem Cells on Proliferation and Apoptosis Mechanisms in Chronic Kidney Disease in the Rat.

Background And Objectives: The feature of chronic kidney failure (CKF) is loss of kidney functions due to erosion of healthy tissue and fibrosis. Recent studies showed that Mesenchymal stem cells (MSCs) differentiated into tubular epithelial cells thus renal function and structures renewed.Furthermore, MSCs protect renal function in CKF.

Rapamycin administration during normal and diabetic pregnancy effects the mTOR and angiogenesis signaling in the rat placenta.

Objective: The mammalian target of rapamycin (mTOR) signaling pathway has newly been recommended to be a nutrient sensor in the placenta. It is speculated that mTORC1 may be activated in diabetes, associated with increased placental nutrient availability. Thus, we aimed to investigate the mTOR signaling pathway both in diabetic and non-diabetic placenta and searched for the alterations of angiogenic factors VEGF, VEGFR1 and VEGFR2.

Effect of glucocorticoids on mechanisms of placental angiogenesis.

The benefits of antenatal glucocorticoid (GC) treatment to promote human fetal lung maturation are well established. However, reports have emerged indicating that maternal exposure to high concentrations of circulating GCs alters placental and fetal development. Because many adult-onset metabolic and cardiovascular disorders have their origins in utero, the importance of prenatal conditions should be considered in detail.

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.

Determination of PCNA, cyclin D3, p27, p57 and apoptosis rate in normal and dexamethasone-induced intrauterine growth restricted rat placentas.

Intrauterine growth restriction (IUGR) is a major clinical problem, which causes perinatal morbidity and mortality. One of the reasons for IUGR is abnormal placentation. In rats, fetal-placental exposure to maternally administered glucocorticoids decreases birth weight and placental weight.

Glucocorticoid exposure altered angiogenic factor expression via Akt/mTOR pathway in rat placenta.

During pregnancy, glucocorticoids (GCs) are used for fetal lung maturation in women at risk of preterm labor. Exogenous GCs do not have exclusively beneficial effects and repeated use of GCs remains controversial. It has been observed that GC exposed rats have smaller placentas and intrauterine growth retarded fetuses.

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

Placenta is a transitional area making many physiological activities between mother and fetus and therefore, it is a critical organ influencing the outcome of pregnancy. Fetal growth is directly related to placental development. Accurate placental development depends on coordinated action of trophoblasts' proliferation, differentiation and invasion.

Location of proliferating cell nuclear antigen and p53 protein in human first trimester and term placenta.

Objective: To examine immunohistochemically the distribution of cell-cycle regulators p53 and proliferating cell nuclear antigen (PCNA), which are in close cooperation with each other in first trimester and term human placentas.

Study Design: Human first trimester placental tissue was obtained by curettage from legal abortions obtained for social reasons, and human term placental tissue was obtained. Neither the interrupted pregnancy nor the obstetrical history showed any abnormalities.

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 diabetes-induced 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.

Immunolocalization of cell cycle proteins (p57, p27, cyclin D3, PCNA and Ki67) in intrauterine growth retardation (IUGR) and normal human term placentas.

Placental development involves a series of events that depend on the coordinated action of proliferation, differentiation and invasion of trophoblasts. Studies on cell cycle related proteins controlling these events are fairly limited. It is still not fully determined how placental tissue proliferation is affected by intrauterine growth retardation (IUGR).

Immunohistochemical distribution of cell cycle proteins p27, p57, cyclin D3, PCNA and Ki67 in normal and diabetic human placentas.

The placenta is a regulator organ for many metabolic activities between mother and fetus. Therefore, fetal growth is directly related to the placental development. Placental development is a series of events that depend on the coordinated action of trophoblasts' proliferation, differentiation and invasion.

Triamcinolone up-regulates GLUT 1 and GLUT 3 expression in cultured human placental endothelial cells.

The placenta is a glucocorticoid target organ, and glucocorticoids (GCs) are essential for the development and maturation of fetal organs. They are widely used for treatment of a variety of diseases during pregnancy. In various tissues, GCs have regulated by glucose transport systems; however, their effects on glucose transporters in the human placental endothelial cells (HPECs) are unknown.

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

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.

Expression of glucocorticoid receptor and glucose transporter-1 during placental development in the diabetic rat.

In various tissues, glucocorticoids (GCs) are known to downregulate glucose transport systems; however, their effects on glucose transporters (GLUTs) in the placenta of a diabetic rat are unknown. Glucocorticoid hormone action within the cell is regulated by the glucocorticoid receptor (GR). Thus, this study was designed to investigate the relationship between GR and glucose transporter expression in the placenta of the diabetic rat.

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

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.

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

Intrauterine growth restriction (IUGR) is a major clinical problem which causes perinatal morbidity and mortality. Although fetuses with IUGR form a heterogeneous group, a major etiological factor is abnormal placentation. Despite the fact that placental development requires the coordinated action of trophoblast proliferation and differentiation, there are few studies on cell cycle regulators, which play the main roles in the coordination of these events.