Atherosclerosis
Study data from University of Alabama update knowledge of atherosclerosis
Published in Blood Weekly, May 21st, 2009
"Deletion of the lysophospholipid-sensitive receptor, G2A, in low-density lipoprotein receptor knockout (LDLR-/-) mice elevates plasma high-density lipoprotein (HDL) cholesterol and suppresses atherosclerosis. However, chemotactic action of G2A in monocytes/macrophages, in addition to its modulatory effect on HDL, may contribute to the proatherogenic action of G2A," investigators in the United States report.
"We determined that deletion of G2A in LDLR-/- mice increases the ApoA1, ApoE, and cholesterol content of plasma HDL fractions. Hepatocytes were shown to express G2A and hepatocytes from G2A-deficient LDLR-/- mice secreted more ApoA1 and ApoE in HDL fractions...
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Source: Blood Weekly (2009-05-21)
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