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JCI online early table of contents: Feb. 8, 2010
Date:2/8/2010

As deletion of Usag1 in Col4a3/ mice led to substantial attenuation of disease progression, preservation of kidney function, and extension of life span, the authors suggest that inhibiting USAG-1 might be a promising therapeutic approach for the treatment of Alport syndrome.

TITLE: Loss of the BMP antagonist USAG-1 ameliorates disease in a mouse model of the progressive hereditary kidney disease Alport syndrome

AUTHOR CONTACT:
Motoko Yanagita
Kyoto University Graduate School of Medicine, Kyoto, Japan.
Phone: 81.75.753.9310; Fax: 81.75.753.9311; E-mail: motoy@kuhp.kyoto-u.ac.jp.

View this article at: http://www.jci.org/articles/view/39569?key=c3580c682d75b2b119bd


HEMATOLOGY: Role for the protein HIF-2-alpha in Chuvash polycythemia

Individuals with a condition known as Chuvash polycythemia, which is caused by a specific mutation in the protein VHL, have a greater proportion of their blood volume occupied by red blood cells than do healthy individuals. They also have pulmonary hypertension (i.e., increased blood pressure in the blood vessels that go to and from the lung) and increased respiratory rates, although the mechanistic basis for these symptoms has not been determined. Now, Celeste Simon and colleagues, at the University of Pennsylvania School of Medicine, Philadelphia, have identified a role for the protein HIF-2-alpha in the lung complications of Chuvash polycythemia by studying mice that model the condition. Of particular interest, HIF-2-alpha activity was found to be increased in lungs from mice that model Chuvash polycythemia. Further, as loss of one copy of the gene responsible for generating HIF-2-alpha in mice that model Chuvash polycythemia suppressed both the polycythemia and pulmonary hypertension, the authors suggest that inhibiting HIF-2-alpha mig
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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