JCI online early table of contents: Jan. 10 2008

EDITOR'S PICK: A new way to boost red blood cell numbers

A common treatment for anemia — a deficiency in red blood cells (rbcs) caused by their insufficient production, excessive destruction, or excessive loss — is administration of recombinant erythropoietin (Epo), a hormone that stimulates the production of rbc precursors by the bone marrow. Unfortunately, many patients with anemia do not respond to treatment with Epo. However, a new study in mice, by Anne Angelillo-Scherrer and her colleagues at the University Hospital Center and University of Lausanne, Switzerland, has indicated that the protein Gas6 might augment or replace Epo in the treatment of patients who are hyporesponsive or resistant to Epo, respectively.

It was shown that following treatment with Epo, mouse rbc precursors released Gas6, which increased cell signaling in response to Epo treatment. In addition, mice deficient in Gas6 had decreased sensitivity to Epo and a reduced ability to recover from anemia. Administration of Gas6, either alone or in combination with Epo, was successful at treating both chronic and acute anemia in mice. The authors therefore concluded that Gas6 has a role in rbc formation and might have valuable therapeutic potential for the treatment of individuals with anemia who fail to respond to treatment with Epo.

TITLE: Role of Gas6 in erythropoiesis and anemia in mice

AUTHOR CONTACT:
Anne Angelillo-Scherrer
University Hospital Center and University of Lausanne, Lausanne, Switzerland.
Phone: 41-21-314-42-22; Fax: 41-21-314-41-80; E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=30375

EDITOR'S PICK: A PIN(1) prick for lung scarring: inhibiting PIN1 reduces rodent lung scarring

Chronic asthma often results in scarring of the lung airways (airway fibrosis) and this can cause airway obstruction. The soluble factor TGF-beta-1, produced by inflammatory cells known as eosinophils, has been shown to drive the processes that result in airway fibrosis, notably fibroblast proliferation and extracellular matrix deposition. Now, James Malter and colleagues at the University of Wisconsin School of Medicine and Public Health, Madison, have generated new data in rodents that has led them to suggest that targeting the protein PIN1 might provide a new approach to limiting airway fibrosis driven by the production of TGF-beta-1 by activated eosinophils in individuals with chronic asthma. These data include the following two observations: first, that pharmacologic blockade of PIN1 in a rat model of chronic asthma reduced TGF-beta-1 expression by activated eosinophils and airway fibrosis; and second, that mice lacking PIN1 showed reduced airway fibrosis when chronically exposed to an allergen.

TITLE: Pin1 regulates TGF-beta-1 production by activated human and murine eosinophils and contributes to allergic lung fibrosis

AUTHOR CONTACT:
James S. Malter
University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Phone: (608) 262-8888; Fax: (608) 265-0367; E-mail: .