Ovarian follicles luteinize following ovulation, requiring structural and molecular remodeling along with exponential increases in steroidogenesis. Cholesterol substrates for luteal steroidogenesis are imported via scavenger receptor-BI (SR-BI) and the low density lipoprotein receptor from circulating high and low density lipoproteins (HDL and LDL) respectively. SR-BI mRNA is expressed in pig ovaries at all stages of folliculogenesis and of the corpus luteum (CL). An 82 kDa form of SR-BI predominates throughout, weakly present in granulosa cells, and robustly expressed in the CL, along with the less abundant 57 kDa form. Digestion of N-linked carbohydrates substantially reduced the SR-BI mass in luteal cells, indicating differences between forms is attributable to glycosylation. Immunohistochemistry revealed SR-BI concentrated in the cytoplasm of follicular granulosa cells while mostly at the periphery of luteal cells. To examine receptor dynamics during gonadotropin-induced luteinization, pigs were treated with an ovulatory stimulus, and ovaries were collected at intervals to ovulation. SR-BI in granulosa cell cytoplasm increased through the peri-ovulatory period, with migration to the cell periphery as the CL matured. In vitro culture of follicles with hCG induced time-dependent upregulation of 82 kDa SR-BI in granulosa cells. SR-BI and LDL receptor were reciprocally expressed, with the latter highest in follicular granulosa cells, declining precipitously with CL formation. We conclude that luteinization causes upregulation of SR-BI expression, its post-translational maturation by glycosylation and insertion into luteal cell membranes. Expression of the LDL receptor is extinguished during luteinization, indicating dynamic regulation of cholesterol importation to maintain elevated steroid output by the CL.