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JCI online early table of contents: Oct. 18, 2010
Date:10/18/2010

.265.2165; Fax: 81.76.234.4223; E-mail: linakura@med.kanazawa-u.ac.jp.

View this article at: http://www.jci.org/articles/view/42315?key=93bbccb990881af23874


NEPHROLOGY: Understanding the mechanism of a classic experimental model of kidney disease

A team of researchers, led by Ali Gharavi, at Columbia University College of Physicians and Surgeons, New York, has provided new insight into the underlying mechanism of kidney injury in a classic experimental model of kidney disease.

Administration of Adriamycin, a chemotherapeutic drug commonly used in the treatment of a wide range of cancers, to certain mouse strains leads to the development of kidney disease. Susceptibility to kidney disease has been mapped to a specific region of mouse chromosome 16. In the study, Gharvi and colleagues were able to more finely map susceptibility to the Prkdc gene. Consistent with this, overexpression of Pkrdc in mouse kidney cells known as podocytes improved their survival after exposure to Adriamycin. Further analysis suggested that Pkrdc helps maintain mitochondrial DNA and that Prkdc might be a modifier gene in human mitochondrial DNA depletion syndromes.

TITLE: Prkdc participates in mitochondrial genome maintenance and prevents Adriamycin-induced nephropathy in mice

AUTHOR CONTACT:
Ali G. Gharavi
Columbia University College of Physicians and Surgeons, New York, New York, USA.
Phone: 212.851.5556; Fax: 212.305.5520; E-mail: ag2239@columbia.edu.

View this article at: http://www.jci.org/articles/view/43721?key=2b5bd382a45e8bafe6c8


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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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