PECAM-1 engagement counteracts ICAM-1-induced signaling in brain vascular endothelial cells

Interactions between leukocytes and vascular endothelial cells are mediated by a complex set of membrane adhesion molecules which transduce bi-directional signals in both cell types. Endothelium of the cerebral blood vessels, which constitute the blood–brain barrier, strictly controls adhesion and trafficking of leukocytes into the brain. Investigating signaling pathways triggered by the engagement of adhesion molecules expressed on brain endothelial cells, we previously documented the role of ICAM-1 in activation of the tyrosine phosphorylation of several actin-binding proteins and subsequent rearrangements of the actin cytoskeleton. In the present study, we show that, whereas PECAM-1 is known to control positively the trans-endothelial migration of leukocytes via homophilic interactions between leukocytes and endothelial cells, PECAM-1 engagement on brain endothelial surface unexpectedly counteracts the ICAM-1-induced tyrosine phosphorylation of cortactin and rearrangements of the actin cytoskeleton. We present evidence that the PECAM-1-associated tyrosine phosphatase SHP-2 is required for ICAM-1 signaling, suggesting that its activity might crucially contribute to the regulation of ICAM-1 signaling by PECAM-1. Our findings reveal a novel activity for PECAM-1 which, by counteracting ICAM-1-induced activation, could directly contribute to limit activation and maintain integrity of brain vascular endothelium

Effects of exposing chicken eggs to a cell phone in "call" position over the entire incubation period

International audienceThe aim of the present study was to assess the effects of exposing fertile chicken eggs to a cell phone repeatedly calling a ten-digit number at 3-min intervals over the entire period of incubation. A pre-experiment was performed first to adjust incubation conditions in an experimental chamber devoid of metallic content and without automatic turning until the overall performance of hatchability was reproducible in the absence of the cell phone. The experimental period consisted of a series of 4 incubations referred to as "replicates". For each replicate, one batch of 60 eggs was exposed to the immediate environment (<= 25 cm) of a cell phone in the "call" position (exposed group), while another batch of 60 eggs, 1.5 m away from the exposed group and also in the incubation chamber, was exposed to a similar cell phone in the "off " position (sham group). For each replicate, 2 other groups each of 60 eggs were also incubated, one in a standard mini-incubator ("Control I" group) and the second in a standard medium size incubator ("Control II" group). Temperature, relative humidity and electromagnetic fields in the experimental chamber were permanently monitored over the entire experiment. A significantly higher percentage of embryo mortality was observed in the "exposed" compared to the "sham" group in 2 of the 4 replicates (p < .05). In comparison with control groups, additional embryo mortality in the exposed group occurred mainly between Days 9 and 12 of incubation but a causal relationship between the intensity of the electric field and embryo mortality could not be established. <= 2008 Elsevier Inc. All rights reserved

Hepatocellular carcinoma in the context of non-alcoholic steatohepatitis (NASH): recent advances in the pathogenic mechanisms

International audienceHepatocellular carcinoma (HCC) is the most common type of liver cancer. HCC is particularly aggressive and is one of the leading causes of cancer mortality. In recent decades, the epidemiological landscape of HCC has undergone significant changes. While chronic viral hepatitis and excessive alcohol consumption have long been identified as the main risk factors for HCC, non-alcoholic steatohepatitis (NASH), paralleling the worldwide epidemic of obesity and type 2 diabetes, has become a growing cause of HCC in the US and Europe. Here, we review the recent advances in epidemiological, genetic, epigenetic and pathogenic mechanisms as well as experimental mouse models that have improved the understanding of NASH progression toward HCC. We also discuss the clinical management of patients with NASH-related HCC and possible therapeutic approaches

Le développement : idéologies et pratiques : actes du séminaire interdisciplinaire de l'ORSTOM (1978-1981) : 1ère partie : évolution des discours sur le développement et les sociétés à développer

India - Tubria instrument for charming snakesColorVolume 129, Page 1

Kaposi's Sarcoma-Associated Herpesvirus-G Protein-Coupled Receptor-Expressing Endothelial Cells Exhibit Reduced Migration and Stimulated Chemotaxis by Chemokine Inverse Agonists

A constitutively active G protein-coupled receptor (GPCR) encoded by Kaposi's sarcoma-associated herpesvirus (human herpesvirus-8) (KSHV) is expressed in endothelial (spindle) cells of Kaposi's sarcoma lesions. In this study, we report novel effects of basal signaling by this receptor and of inverse agonist chemokines on migration of KSHV-GPCR-expressing mouse lung endothelial cells. We show that basal signaling by KSHV-GPCR inhibits migration of endothelial cells in two systems, movement through porous filters and in vitro wound closure. Naturally occurring chemokines, interferon γ-inducible protein-10 and stromal-derived factor-1, which act as inverse agonists at KSHV-GPCR, abrogate the inhibition of migration and stimulate directed migration (or chemotaxis) of these cells. Thus, the expression of KSHV-GPCR may allow infected endothelial cells in situ to remain in a localized environment or to directionally migrate along a gradient of specific chemokines that are inverse agonists at KSHV-GPCR

Esquisse d'un programme

Aubertin Catherine, Cabanes Robert, Chauveau Jean-Pierre, Pontié Guy, Robineau Claude, Couty Philippe. Esquisse d'un programme. In: Tiers-Monde, tome 23, n°90, 1982. Sociologie du développement, sous la direction de Yves Goussault. pp. 335-344