Ethanol alters proliferation and differentiation of normal and chromosomally abnormal human embryonic stem cell-derived neurospheres.

Ethanol is a powerful substance and, when consumed during pregnancy, has significant psychoactive and developmental effects on the developing fetus. These abnormalities include growth retardation, neurological deficits, and behavioral and cognitive deficiencies, commonly referred to as fetal alcohol spectrum disorder. The effect of ethanol has been reported to affect cellular development on the embryonic level, however, not much is known about mutations contributing to the influence of ethanol.

Lectins identify glycan biomarkers on glioblastoma-derived cancer stem cells.

Glioblastoma (GBM) is a highly aggressive primary brain tumor with a poor prognosis. Despite aggressive therapy with surgery, radiotherapy, and chemotherapy, nearly all patients succumb to disease within 2 years. Several studies have supported the presence of stem-like cells in brain tumor cultures that are CD133-positive, are capable of self-renewal, and give rise to all cell types found within the tumor, potentially perpetuating growth.

Human embryonic stem cell model of ethanol-mediated early developmental toxicity.

Background: Fetal alcohol syndrome is an important clinical problem. Human embryonic stem cells (hESC) have not been widely used to study developmental alcohol toxicity. Here we document the phenotype of hESC exposed to clinically-relevant, low dose ethanol (20mM).

GABRB3 gene expression increases upon ethanol exposure in human embryonic stem cells.

Ionotropic receptors are the target for most mood-defining compounds. Chronic exposure to ethanol (EtOH) alters receptor-mediated responses and the numbers of these channels and specific subunits; as well as induces anxiolytic, sedative, and anesthetic activity in the human brain. However, very little is known regarding the effects of EtOH on ionotropic receptor transcription during early human development (preimplantation).

Low ethanol concentration alters CHRNA5 RNA levels during early human development.

Alcohol use is common and consumption during pregnancy has been shown to lead to a myriad of physical and neurologic abnormalities commonly referred to as fetal alcohol spectrum disorder. Substance addiction, which includes alcohol, has been shown to involve the major nicotinic acetylcholine receptor subunit CHRNA5. Using human embryonic stem cells as a model of early human development, we show that low concentrations of ethanol (20mM) can alter the expression of CHRNA5.

Heparin binding epidermal growth factor-like growth factor and PD169316 prevent apoptosis in mouse embryonic stem cells.

Apoptosis or programmed cell death is an important outcome of cell fate and is influenced by several factors. Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a member of the EGF family of growth factors and is synthesized as a membrane-associated precursor molecule (proHB-EGF). Under stressful conditions proHB-EGF is proteolytically cleaved and released as a soluble ligand (sHB-EGF) that activates the EGF receptor.

Heat shock proteins, endothelin, and peripheral neuronal injury.

Heat shock proteins (HSP) are important in neuroprotection after a variety of stresses or injuries. Both heat shock proteins and endothelin are upregulated after peripheral nerve injury, but HSP regulation after injury has not been systematically studied in peripheral nerve. The purpose of this study was to examine the regulation of small and large heat shock proteins after injury to rat sciatic nerve.

Activin a efficiently specifies definitive endoderm from human embryonic stem cells only when phosphatidylinositol 3-kinase signaling is suppressed.

Human ESCs (hESCs) respond to signals that determine their pluripotency, proliferation, survival, and differentiation status. In this report, we demonstrate that phosphatidylinositol 3-kinase (PI3K) antagonizes the ability of hESCs to differentiate in response to transforming growth factor beta family members such as Activin A and Nodal. Inhibition of PI3K signaling efficiently promotes differentiation of hESCs into mesendoderm and then definitive endoderm (DE) by allowing them to be specified by Activin/Nodal signals present in hESC cultures.