Estrogen regulation of the scavenger receptor class B gene: Anti-atherogenic or steroidogenic, is there a priority?

High density lipoprotein (HDL) participates in reverse cholesterol transport and in the delivery of cholesterol to the liver and steroidogenic tissues by a mechanism called "selective lipid uptake" which is mediated by the HDL receptor, scavenger receptor B type I (SR-BI). Overexpression of SR-BI suppresses atherosclerosis by increasing reverse cholesterol transport. In contrast, genetic ablation of SR-BI has a negative effect on cardiovascular physiology in both males and females and a gender specific negative impact on female fertility. Cholesterol is essential for mammalian embryonic development as a necessary component of cell membranes and as a substrate for steroidogenesis. The SR-BI receptor is highly expressed in the human placenta allowing the growing fetus to obtain a considerable portion of cholesterol from maternal lipoproteins. Estrogen, which plays an important role in maintaining pregnancy, has been shown to enhance plasma HDL levels and promote reverse cholesterol transport. Since SR-BI is the major determinant of serum HDL levels, direct regulation of the SR-BI gene by estrogen is theorized. The objective of this manuscript is to summarize the current information related to estrogen regulation of the gene that codes for the SR-BI receptor.