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(Circulation Research. 2002;90:244.)
© 2002 American Heart Association, Inc.

Editorials

MIghty Mouse

Alan R. Tall

From the Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY.

Correspondence to Alan R. Tall, Division of Molecular Medicine, Dept of Medicine, Columbia University, New York, NY 10032. E-mail art1@columbia.edu

Key Words: atherosclerosis • myocardial infarction • mouse • scavenger receptor-BI

A mouse with spontaneous coronary atherosclerosis and myocardial infarction (MI) would be a wonderful research tool. In this issue of Circulation Research, Braun et al¹ show that young mice with combined deficiencies of apolipoprotein E (apoE) and the scavenger receptor-BI (SR-BI) spontaneously develop severe coronary atherosclerosis, myocardial infarction, and cardiac dysfunction. Although much remains to be learned about the underlying mechanisms, it is clear that this study represents an important step toward developing an authentic mouse model of coronary occlusion and human myocardial infarction. These animals are likely to be useful for studying the effects of genetic or other interventions on these disease processes.

SR-BI was originally identified by expression cloning and shown to bind both native and modified LDL.² Insightfully, Krieger and colleagues³ then showed that SR-BI can also bind HDL and mediate the selective cellular uptake of HDL cholesteryl ester without degradation of HDL protein, ie, selective uptake. Selective uptake of HDL cholesteryl esters in tissues had been described more than a decade earlier by lipoprotein physiologists who showed that the process was most active in rodent liver and adrenals.⁴ These organs are also the principal sites of SR-BI expression, and mice with decreased SR-BI expression have increased HDL levels^5,6 and decreased selective uptake.⁶ When crossed with apoE⁷ or LDL receptor knockout (KO) mice,⁸ the SR-BI deficient mice were found to have increased atherosclerosis in the aortic root. Conversely, mice with hepatic overexpression of SR-BI tended to have reduced HDL levels and diminished aortic atherosclerosis.^9,10

In the . . . [Full Text of this Article]

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