Dec. 15, 2007 Atherosclerosis is an inflammatory disease of the arterial blood vessels enhanced by the presence of immune cells known as macrophages. Macrophages migrate to the cholesterol-rich atherosclerotic plaques that form in the blood vessels and are the central component of atherosclerotic disease.
Phospholipase C (PLC) is a protein that has known importance in immune cell signaling, although no specific known function in atherosclerosis.
But now, Dianqing Wu and colleagues from Yale University School of Medicine, New Haven, have discovered that the beta-3 form of PLC plays an important role in encouraging macrophage survival within atherosclerotic plaques.
The authors generated mice deficient in PLC-beta-3. Although macrophages from these mice retained many of their normal functions, they were hypersensitive to inducers of a form of cell death known as apoptosis. Mice deficient in the protein apoE are more susceptible to atherosclerosis than normal mice. In the study, mice deficient in both apoE and PLC-beta-3 proteins were shown to have fewer macrophages within their atherosclerotic plaques, more macrophage apoptosis within the plaques, and smaller atherosclerotic plaques compared to mice deficient in apoE alone.
Because only macrophages appeared to be effected by the PLC-beta-3 deficiency, and because the effect on these macrophages seemed to be limited to their sensitivity to apoptosis, the authors concluded that PLC-beta-3 might provide a new therapeutic target in the prevention of atherosclerosis.
Article: Phospholipase C beta-3 deficiency leads to macrophage hypersensitivity to apoptotic induction and reduction of atherosclerosis in mice. Journal of Clinical Investigation. Dec 14, 2007.
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