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.
“Inflammatory macrophage migration requires MMP-9 activation by plasminogen in mice”
Yanqing Gong, Erika Hart, Aleksey Shchurin and Jane Hoover-Plow
J. Clin. Invest. doi:10.1172/JCI32750.
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The Journal of Clinical Investigation (JCI) is the publication of the American Society for Clinical Investigation, an honor society of physician-scientists.
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