JCI online early table of contents: Au...(E: Leukemia-associated NOTCH1 alleles ar...),Health

AUTHOR CONTACT:
Warren S. Pear
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 573-7764; Fax: (215) 573-6725; E-mail: wpear@mail.med.upenn.edu.

Jon C. Aster
Brigham and Women's Hospital, Boston, Massachusetts, USA.
Phone: (617) 525-7329; Fax: (617) 264-5169; E-mail: jaster@rics.bwh.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=35090

New insight into the way in which inflammatory cells known as macrophages leave the blood and access sites of injury has been provided by Jane Hoover-Plow and colleagues, at Cleveland Clinic Lerner Research Institute, Cleveland, who studied the process in mice. This information has particular clinical relevance to injury and inflammation of the major arterial blood vessels, one of the main causes of heart attack and stroke.

It was found that in mice lacking a protein known as plasminogen, macrophages were less able to leave the blood and access sites of injury than in normal mice. This was associated with decreased activation of a protein known as MMP-9, and addition of MMP-9 to the mice restored the ability of macrophages to access sites of injury. As this was also true in a mouse model of abdominal aortic aneurysm (AAA), a chronic degenerative condition of the aorta that is usually fatal if it ruptures, the authors suggest that targeting the plasminogen/MMP-9 pathway might be a viable approach to controlling disease-causing inflammation, such as occurs in the development of AAA.

TITLE: Inflammatory macrophage migrati
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