Maintenance of pluripotency and self-renewal ability of mouse embryonic stem cells in the absence of tetraspanin CD9.

We have previously demonstrated that the tetraspanin CD9 is necessary for membrane fusion between sperm and oocyte during fertilization. While knockout mice for CD9 are viable, CD9(-/-) females are sterile due to the inability of their oocytes to fuse with sperm. While CD9 is not essential for subsequent development, a role in embryonic stem (ES) cell self-renewal was hypothesised on the basis of two observations: CD9 is highly expressed in murine and human ES cells and the CD9-blocking antibody inhibits mouse ES cell colony formation and survival.

Shortening of human cell life span by induction of p16ink4a through the platelet-derived growth factor receptor beta.

Mesenchymal stem cells (MSCs) are attracting a great deal of attention because they represent a valuable source of cells for use in regenerative medicine. In human cell culture it is important to obtain large numbers of cells for use in therapy. In this study, we attempted to prolong life span of a marrow-derived mesenchymal stem cell using a combination of growth factors and hormones.

Insulin hypersensitivity in mice lacking the V1b vasopressin receptor.

We have reported that [Arg(8)]-vasopressin-stimulated insulin release is blunted in islet cells isolated from V1b receptor-deficient (V1bR(-/-)) mice. In this study, we used V1bR(-/-) mice to examine the physiological role of the V1b receptor in regulating blood glucose levels in vivo, and we found that the fasting plasma glucose, insulin and glucagon levels were lower in V1bR(-/-) mice than in wild-type (V1bR(+/+)) mice. Next, we evaluated glucose tolerance by performing an intraperitoneal glucose tolerance test (GTT).

Impaired arginine-vasopressin-induced aldosterone release from adrenal gland cells in mice lacking the vasopressin V1A receptor.

We examined aldosterone release in response to stimulation with arginine-vasopressin (AVP) using adrenal gland cells. AVP caused a significant increase in aldosterone release from the dispersed adrenal gland cells of wild-type mice (V1AR+/+) at concentrations from 0.1 microM to 1 microM.

Blockade of both alpha1A- and alpha1B-adrenergic receptor subtype signaling is required to inhibit neointimal formation in the mouse femoral artery.

Attenuation of early restenosis after percutaneous coronary intervention (PCI) is important for the successful treatment of coronary artery disease. Some clinical studies have shown that hypertension is a risk factor for early restenosis after PCI. These findings suggest that alpha(1)-adrenergic receptors (alpha(1)-ARs) may facilitate restenosis after PCI because of alpha(1)-AR's remarkable contribution to the onset of hypertension.

Alteration of glucose homeostasis in V1a vasopressin receptor-deficient mice.

Arginine-vasopressin (AVP) is known to be involved in maintaining glucose homeostasis, and AVP-resistance is observed in poorly controlled non-insulin-dependent diabetes mellitus subjects, resulting in a lowered plasma volume. Recently we reported that V1a vasopressin receptor-deficient (V1aR(-/-)) mice exhibited a decreased circulating blood volume and hypermetabolism of fat accompanied with impaired insulin-signaling. Here we further investigated the roles of the AVP/V1a receptor in regulating glucose homeostasis and plasma volume using V1aR(-/-) mice.

Potential use of embryonic stem cells for the treatment of mouse parkinsonian models: improved behavior by transplantation of in vitro differentiated dopaminergic neurons from embryonic stem cells.

Background: and Aims. The purpose of the present study was to examine the efficacy of transplantation of mouse embryonic-stem-(ES)-cell-derived tyrosine hydroxylase-positive (TH(+)) cells into Parkinsonian mice using behavioral tests and immunohistochemical evaluation.

Methods: Undifferentiated ES cells carrying the enhanced green fluorescent protein (EGFP) gene were differentiated into a cell population containing TH(+) neurons using a five-step in vitro differentiation method.