Angiopoietin-1 mediates inhibition of hypertension-induced release of angiopoietin-2 from endothelial cells.

Aims: Adequate endothelial cell stimulation is a prerequisite for the adaptive remodelling of macro- and microvessels. A pivotal autocrine mechanism following endothelial cell activation is the release of angiopoietin-2 (Ang-2), which subsequently antagonizes the binding of Ang-1 to the Tie-2 receptor, thus sensitizing the endothelial cells to pro-angiogenic and/or pro-inflammatory stimuli. Based on the observation that hypertension in mice reduces the abundance of Ang-2 stored in arterial endothelial cells, this study was aimed at testing the hypothesis that an increase in wall stress (WS) or stretch-a hallmark of hypertension-is sufficient to release Ang-2 from endothelial cells.

VEGF overexpression improves mice cognitive abilities after unilateral common carotid artery occlusion.

Angiogenesis and neurogenesis are adaptive responses protecting cerebral tissue from hypoxic-ischemic injury. Both processes seem to be governed by hypoxia-induced growth factors, of which vascular endothelial growth factor (VEGF) is a prominent example. The aim of this study was to investigate the influence of VEGF overexpression (V1 mice) on mice cognitive function and cerebral structure under moderate cerebral oligemia.

Flow-dependent regulation of angiopoietin-2.

Endothelial cells are constantly exposed to high or low shear stress in arteries and veins by the flowing blood. Angiopoietin-2 (Ang-2) is acting as a critical regulator of vessel maturation and endothelial cell quiescence. In this study, flow-dependent regulation of Ang-2 was analyzed in vitro and in vivo.

Generation of inducible hepatitis C virus transgenic mouse lines.

Hepatitis C virus (HCV) is the causative agent of most cases of chronic liver disease, cirrhosis, and hepatocellular carcinoma (HCC) affecting more than 170 million people world-wide. Progress in elucidating the nature of HCV and the development of new therapeutic strategies is hampered fundamentally by the absence of adequate small animal models simulating natural HCV infection. The creation of conditional mouse lines with the tetracycline-controlled gene expression system holds new perspectives for simulation of wild-type HCV infection in a small animal model.

Induction of antigen-specific immune responses in vivo after vaccination with dendritic cells transduced with adenoviral vectors encoding hepatitis C virus NS3.

Dendritic cells (DC) are potent antigen-presenting cells that play a critical role in the initiation of immunity to viral infections. Direct transduction of DC appears to be the major pathway in vivo responsible for induction of antigen specific immune responses. The aim of this study was to explore the vaccine potential of DC transduced with adenoviral vectors encoding the HCV nonstructural protein 3 (AdNS3) compared to DC pulsed with recombinant NS3 (rNS3).

Multigenotype HCV-NS3 recombinant vaccinia viruses as a model for evaluation of cross-genotype immunity induced by HCV vaccines in the mouse.

Surrogate infections with HCV-recombinant vaccinia viruses (HCV-rVV) are a standard method to test the efficacy of hepatitis C virus (HCV) vaccine candidates in the mouse model. We established a panel of 16 HCV-rVV expressing the nonstructural protein 3 (NS3) of HCV genotypes 1a, 1b, 2, 3 and 4. Mice immunized with recombinant NS3 protein derived from HCV genotype 1b were challenged with the rVV.