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JCI online early table of contents: June 13, 2011
Date:6/13/2011

es phosphodiesterases (PDEs). In this study, Fischmeister, Vandecasteele, and colleagues have identified a role for PDE4B in limiting LTCC opening in mouse heart muscle cells and determined that this prevents arrhythmias. As decreased levels of PDE4b were recently observed in failing hearts, the authors suggest that their new data provide a mechanistic link between arrhythmias and sudden death in individuals with heart failure.

TITLE: Phosphodiesterase 4B in the cardiac L-type Ca2+ channel complex regulates Ca2+ current and protects against ventricular arrhythmias in mice

AUTHOR CONTACT:
Rodolphe Fischmeister
INSERM UMR-S 769, Universit Paris-Sud, Chtenay-Malabry, France.
Phone: 33.1.46.83.57.57; Fax 33.1.46.83.54.75; E-mail: rodolphe.fischmeister@inserm.fr.

Grgoire Vandecasteele
INSERM UMR-S 769, Universit Paris-Sud, Chtenay-Malabry, France.
Phone: 33.1.46.83.57.57; Fax 33.1.46.83.54.75; E-mail: gregoire.vandecasteele@u-psud.fr.

View this article at: http://www.jci.org/articles/view/44747?key=0c65036b7be373cd725d


HEMATOLOGY: The protein P2X7 receptor triggers blood clot formation

Injury to blood vessel walls triggers the formation of a blood clot (thrombus). Clinically, many conditions are linked to unwanted thrombus formation (e.g., heart attack, DVT, and stroke) and antiblood clotting therapies (anticoagulants) are used widely. A potential new approach to anti-coagulant therapy is provided by work in mice performed by a team of researchers, led by Wolfram Ruf, at the Scripps Research Institute, La Jolla.

Thrombus formation is triggered by the protein TF, which is expressed on blood vessel walls, blood cells known as myeloid cells, and myeloid cellderived microparticles. How thr
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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