Inactivating a protein that helps regulate the proliferation of vascular cells increases the chance of developing atherosclerosis, a major cause of heart disease, researchers at UT Southwestern Medical Center at Dallas have discovered.
Vascular vessels endure constant pounding and considerable stresses associated with blood flow. Vascular smooth muscle cells play an important role in the development of blood vessels, providing structural integrity and the ability to dilate and constrict. The low-density lipoprotein receptor-related protein (LRP1) helps regulate the proliferation and movement of these smooth muscle cells, presumably because LRP1 forms a complex with the receptor for platelet-derived growth factor (PDGF).
In findings reported in today’s issue of Science, a UT Southwestern research team led by Dr. Joachim Herz, professor of molecular genetics and in the Center for Basic Neuroscience, discovered that inactivating LRP1 in vascular smooth muscle cells caused the overexpression of PDGF receptor and abnormal PDGF receptor signaling in mice. Smooth muscle cells proliferated and the vessel wall became highly susceptible to cholesterol buildup.
Susan Morrison | EurekAlert!
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