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AssigneesMassachusetts Institute of Technology, Center for Blood Research, Inc.
InventorsThomas J.F. Neiland, Monty Krieger, Tomas Kirchausen
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Methods for regulation of lipid and cholesterol uptake are described which are based on regulation of the expression or function of the SR-BI HDL receptor. The examples demonstrate that estrogen dramatically downregulates SR-BI under conditions of tremendous upregulation of the LDL-receptor. The examples also demonstrate the upregulation of SR-BI in rat adrenal membranes and other non-placental steroidogenic tissues from animals treated with estrogen, but not in other non-placental non-steroidogenic tissues, including lung, liver, and skin. Examples further demonstrate the uptake of fluorescently labeled HDL into the liver cells of animal, which does not occur when the animals are treated with estrogen. Examples also demonstrate the in vivo effects of SR-BI expression on HDL metabolism, in mice transiently overexpressing hepatic SR-BI following recombinant adenovirus infection. Overexpression of the SR-BI in the hepatic tissue caused a dramatic decrease in cholesterol blood levels. These results demonstrate that modulation of SR-BI levels, either directly or indirectly, can be used to modulate levels of cholesterol in the blood.
A compound which specifically alters the binding activity of SR-BI, in combination with a pharmaceutically acceptable carrier, in an effective amount to treat a human or animal in need thereof, obtained by screening a library of compounds for alteration of SR-B1 binding activity or expression.
A method of identifying a compound which alters SR-BI binding activity or expression comprising screening a library of compounds.
Dependencies are inferred from the claim text.