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Cardiovascular disease (CVD) is the largest cause of premature death in human populations throughout the world. Circulating plasma lipid levels, specifically high levels of LDL or low levels of HDL, are predictive of susceptibility to CVD. The scavenger receptor class B member 1 (SCARB1) is the primary receptor for the selective uptake of HDL cholesterol by liver and steroidogenic tissues. Hepatic SCARB1 influences plasma HDL-cholesterol levels and is vital for reverse cholesterol transport. Here we describe the mapping of a novel  N -ethyl- N -nitrosourea (ENU) induced point mutation in the  Scarb1  gene identified in a C57BL/6J background. The mutation is located in a highly conserved amino acid in the extracellular loop and leads to the conversion of an isoleucine to an asparagine (I179N). Homozygous mutant mice express normal  Scarb1  mRNA levels and are fertile. SCARB1 protein levels are markedly reduced in liver (∼90%), but not in steroidogenic tissues. This leads to ∼70% increased plasma HDL levels due to reduced HDL cholesteryl ester selective uptake.  Pdzk1  knockout mice have liver-specific reduction of SCARB1 protein as does this mutant; however,  in vitro  analysis of the mutation indicates that the regulation of SCARB1 protein in this mutant is independent of PDZK1. This new  Scarb1  model may help further our understanding of post-translational and tissue-specific regulation of SCARB1 that may aid the important clinical goal of raising functional HDL.

Novel ENU-Induced Point Mutation in Scavenger Receptor Class B, Member 1, Results in Liver Specific Loss of SCARB1 Protein