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.

Effects of transcranial direct current stimulation on the glutamatergic pathway in the male rat hippocampus after experimental focal cerebral ischemia.

This study aimed to assess the focal cerebral ischemia-induced changes in learning and memory together with glutamatergic pathway in rats and the effects of treatment of the animals with transcranial Direct Current Stimulation (tDCS). One hundred male rats were divided into five groups as sham, tDCS, Ischemia/Reperfusion (IR), IR + tDCS, and IR + E-tDCS groups. Learning, memory, and locomotor activity functions were evaluated by behavioral experiments in rats.

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 .

Human Trophoblast Progenitor Cells Express and Release Angiogenic Factors.

Trophoblast stem cells develop from polar trophectoderm and give rise to the cells that generate the placenta. Trophoblast cells are responsible for the uterine invasion and vascular remodeling during the implantation of the embryo. However this knowledge is not yet to be confirmed for trophoblast progenitor cells (TPCs).

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.

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 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.

Merit of quinacrine in the decrease of ingested sulfite-induced toxic action in rat brain.

We aimed at investigating the effects of sulfite-induced lipid peroxidation and apoptosis mediated by secretory phospholipase A2 (sPLA2) on somatosensory evoked potentials (SEP) alterations in rats. Thirty male albino Wistar rats were randomized into three experimental groups as follows; control (C), sodium metabisulfite treated (S), sodium metabisulfite+quinacrine treated (SQ). Sodium metabisulfite (100 mg/kg/day) was given by gastric gavage for 5 weeks and 10 mg/kg/day quinacrine was applied as a single dose of intraperitoneal injection for the same period.

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.

The effect of heparin on structural and functional properties of low density lipoproteins.

Heparin binding to human low density lipoproteins (LDL) and the effect of heparin on the ability of LDL to bind to the LDL receptor has been investigated. Emphasis has been made on the physiological conditions of temperature, pH and the ionic strength. Intrinsic fluorescence spectroscopy of LDL has been applied to follow heparin binding.

T-cadherin mediates low-density lipoprotein-initiated cell proliferation via the Ca(2+)-tyrosine kinase-Erk1/2 pathway.

The GPI-anchored protein T-cadherin was found to be an atypical LDL binding site that is expressed in various types of cells, including endothelial cells, smooth muscle cells, and neurons. Notably, the expression of T-cadherin was reduced in numerous types of cancers, although it was up-regulated in tumor-penetrating blood vessels, atherosclerotic lesions, and during neointima formation. Despite these intriguing findings, our knowledge of the physiological role and the signal transduction pathways associated with this protein is limited.

Anandamide initiates Ca(2+) signaling via CB2 receptor linked to phospholipase C in calf pulmonary endothelial cells.

The endocannabinoid anandamide has been reported to affect neuronal cells, immune cells and smooth muscle cells via either CB1 or CB2 receptors. In endothelial cells, the receptors involved in activating signal transduction are still unclear, despite the fact that anandamide is produced in this cell type. The present study was designed to explore in detail the effect of this endocannabinoid on Ca2+ signaling in single cells of a calf pulmonary endothelial cell line.