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JCI table of contents: Nov. 8, 2007
Date:11/8/2007

nd colleagues at the University of Pennsylvania, Philadelphia, has provided new insight into the mechanisms underlying Chuvash polycythemia and should provide a useful tool to assess the efficacy of potential therapies for the treatment of polycythemias.

A specific mutation in the gene that makes the protein VHL causes Chuvash polycythemia. In this study, mice expressing the same mutation (VhlR/R mice) were generated and shown to develop disease that almost recapitulated that observed in individuals with Chuvash polycythemia. The mice exhibited increased activity of the protein HIF-2-alpha in the spleen and this was associated with an increased number of red blood cells in the spleen due to their increased generation at that site. The authors therefore concluded that enhanced expression of HIF-2-alpha promotes the splenic production of red blood cells and that this causes the polycythemia in VhlR/R mice.

TITLE: von HippelLindau mutation in mice recapitulates Chuvash polycythemia via hypoxia-inducible factor-2-alpha signaling and splenic erythropoiesis

AUTHOR CONTACT:
M. Celeste Simon
University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Phone: (215) 746-5532; Fax: (215) 746-5511; E-mail: celeste2@mail.med.upenn.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32614


IMMUNOLOGY: Two faces for TNF-alpha in antiviral and antitumor immunity

Antagonists of the soluble factor TNF-alpha are used to treat individuals with inflammatory and autoimmune diseases mediated by immune cells known as T cells, e.g. rheumatoid arthritis. Despite this there are contradictory reports as to the effects of TNF-alpha on T cell responses. New research in mice by Pamela Ohashi and colleagues at the Ontario Cancer Institute, Toronto, has provided a potential explanation f
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
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