[ Back to EurekAlert! ] Public release date: 10-Jan-2008
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation

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.

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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: jsmalter@wisc.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32789



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