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JCI table of contents: May 24, 2010
Date:5/24/2010

508.856.1094; E-mail: Kenneth.rock@umassmed.edu.

View this article at: http://www.jci.org/articles/view/40124?key=ac91a47573601775e478

ACCOMPANYING COMMENTARY
TITLE: Caught red handed: uric acid is an agent of inflammation

AUTHOR CONTACT:
Yan Shi
University of Calgary, Calgary, Alberta, Canada.
Phone: 403.220.2536; Fax: 403.220.2772; E-mail: yshi@ucalgary.ca.

View this article at: http://www.jci.org/articles/view/43132?key=ad6d1c7bf2d7861e5736


PULMONARY: Natural protection from scarring of the lungs

Pulmonary fibrosis, a medical condition often described as scarring of the lungs, develops as a progressive, dysregulated response to lung injury. One natural process that protects the lung from fibrosis is activation of the protein plasminogen, but how this provides protection has not been determined. Now, a team of researchers, led by Bethany Moore and Marc Peters-Golden, at the University of Michigan, Ann Arbor, has provided insight into this issue by studying the mechanism by which mice lacking an inhibitor of plasminogen activation known as PAI-1 are protected in a model of pulmonary fibrosis. The key finding of the study was that a known antifibrotic mediator, PGE2, was expressed at high levels in the lungs of mice lacking PAI-1 during fibrosis. Further analysis clearly defined the molecular pathway by which increased plasminogen led to PGE2 production. The clinical relevance of these data was highlighted by the observation that cells in the lungs of patients with a form of pulmonary fibrosis known as idiopathic pulmonary fibrosis were unable to increase PGE2 production in response to the production of plasminogen activation.


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