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JCI online early table of contents: Sept. 12, 2011
Date:9/12/2011

E: In vitro differentiation of human macrophages with enhanced antimycobacterial activity

AUTHOR CONTACT:
Guillaume Vogt
The Rockefeller University, New York, New York, USA.
Phone: 212.327.7336; Fax: 212.327.7330; E-mail: guillaume.vogt@inserm.fr.

Carl Nathan
Weill Cornell Medical College, New York, New York, USA.
Phone: 212.746.6505; Fax: 212.746.8587; E-mail: cnathan@med.cornell.edu.

View this article at: http://www.jci.org/articles/view/57235?key=adc45d67924205d0a233


NEPHROLOGY: Defining a molecular mechanism that lacks integrity in the kidney

A key function of our kidneys is to filter waste from our blood and to divert this into our urine. Proteinuric kidney diseases, which are characterized by high levels of protein in the urine, are caused by breakdown of the filtration barrier in the kidney that prevents proteins in the blood from being lost into the urine. In particular, these diseases are caused by injury to podocytes, specialized cells that are key to the integrity of the filtration barrier. A team of researchers led by Sanja Sever, at Massachusetts General Hospital, Boston, and Jochen Reiser, at the University of Miami, Miami has now identified a molecular mechanism that impairs key features of mouse and human podocytes that are essential for their function in the filtration barrier of the kidney. The authors conclude that this molecular mechanism could underlie proteinuric kidney disease and suggest that it provides potential new targets for treatment.

TITLE: CD2AP in mouse and human podocytes controls a proteolytic program that regulates cytoskeletal structure and cellular survival

AUTHOR CONTACT:
Sanja Sever
Massachusetts General Hospital, Harvard Medical School, Bost
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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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