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JCI online ahead of print table of contents for March 18, 2014
Date:3/18/2014

sm will be beneficial for a wide range of metabolic diseases.

TITLE: Bone-specific insulin resistance disrupts whole-body glucose homeostasis via decreased osteocalcin activation

AUTHOR CONTACT: Gerard Karsenty
Columbia University, New York, NY, USA
Phone: 212 305 4011; E-mail: gk2172@columbia.edu

View this article at: http://www.jci.org/articles/view/72323

ACCOMPANYING COMMENTARY TITLE: Insulin, osteoblasts, and energy metabolism: why bone counts calories

AUTHOR CONTACT: Thomas Clemens
Center for Musculoskeletal Research, John Hopkins, Baltimore, MD, USA
Phone: 410.955.3245; E-mail: tclemen5@jhmi.edu

View this article at: http://www.jci.org/articles/view/75554


Pathogenic interactions between platelets and neutrophils are mediated by AKT2

Pathological interactions between blood cells promote thrombo-inflammatory disease and result in complications such as vaso-occlusion during atherothrombosis, inflammation, and ischemia. Activated platelets, leukocytes and endothelial cells all contribute to the development of vaso-occlusion: though how interactions between these cell types are regulated is poorly understood. In this issue of the Journal of Clinical Investigation, Jaehyung Cho and colleagues at the University of Illinois determined that the serine/threonine kinase AKT2 was required for heterotypic aggregation of activated platelets, neutrophils and endothelial cells during TNF-α-induced vascular inflammation. In neutrophils, AKT2 phosphorylation activated and resulted in membrane translocation of αMβ2 integrin, which promoted cell-cell attachment. Neutrophils an
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Contact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

Page: 1 2 3 4 5 6

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