One of the most common causes of death in the developed world is a disease of the major arterial blood vessels that can cause heart attacks and stroke. A critical step in this disease (which is known as atherosclerosis, or hardening of the arteries) is the trapping of cells known as macrophages in the innermost layer of arteries, but the mechanism by which this occurs has not been well defined.
Now, however, Roy Silverstein and colleagues, at the Cleveland Clinic Foundation, Cleveland, have provided insight into this event by studying mice and human macrophages in vitro.
In the study, both in vivo and in vitro assays indicated that a molecule known as oxLDL, which is an important trigger of atherosclerosis, inhibited the migration of mouse macrophages. Importantly, this inhibitory effect was not observed if the macrophages came from mice lacking the protein CD36.
A similar role was also observed for CD36 in modulating the in vitro migratory response of human macrophages to oxLDL.
Further analysis revealed the molecular changes that occur after oxLDL interaction with CD36 to modulate macrophage migration. The authors speculate that the interaction of oxLDL and CD36 on macrophages might inhibit their migration in vivo and lead to them becoming trapped in the innermost layer of the arterial wall.
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