title: Expression of scavenger receptor-BI and low-density lipoprotein receptor and differential use of lipoproteins to support early steroidogenesis in luteinizing macaque granulosa cells.
abstract: An ovulatory hCG stimulus to rhesus macaques undergoing controlled ovarian stimulation protocols results in a rapid and sustained increase in progesterone synthesis. The use of lipoproteins as a substrate for progesterone synthesis remains unclear, and the expression of lipoprotein receptors [very-low-density lipoprotein receptor (VLDLR), low-density lipoprotein receptor (LDLR), and scavenger receptor-BI (SR-BI)] soon after human chorionic gonadotropin (hCG) (<12 h) has not been characterized. This study investigated lipoprotein receptor expression and lipoprotein (VLDL, LDL, and HDL) support of steroidogenesis during luteinization of macaque granulosa cells. Granulosa cells were aspirated from rhesus monkeys undergoing controlled ovarian stimulation before or up to 24 h after an ovulatory hCG stimulus. The expression of VLDLR decreased within 3 h of hCG, whereas LDLR and SR-BI increased at 3 and 12 h, respectively. Granulosa cells isolated before hCG were cultured for 24 h in the presence of FSH or FSH plus hCG with or without VLDL, LDL, or HDL. Progesterone levels increased in the presence of hCG regardless of lipoprotein addition, although LDL, but not HDL, further augmented hCG-induced progesterone. Other cells were cultured with FSH or FSH plus hCG without an exogenous source of lipoprotein for 24 h, followed by an additional 24 h culture with or without lipoproteins. Cells treated with hCG in the absence of any lipoprotein were unable to maintain progesterone levels through 48 h, whereas LDL (but not HDL) sustained progesterone synthesis. These data suggest that an ovulatory stimulus rapidly mobilizes stored cholesterol esters for use as a progesterone substrate and that as these are depleted, new cholesterol esters are obtained through an LDLR- and/or SR-BI-mediated mechanism.
authors.affiliation: Department of Obstetrics, Gynecology, & Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
authors.forename: Mary
authors.initials: M
authors.lastname: Cherian-Shaw
authors.forename: Muraly
authors.initials: M
authors.lastname: Puttabyatappa
authors.forename: Erin
authors.initials: E
authors.lastname: Greason
authors.forename: Annabelle
authors.initials: A
authors.lastname: Rodriguez
authors.forename: Catherine A
authors.initials: CA
authors.lastname: VandeVoort
authors.forename: Charles L
authors.initials: CL
authors.lastname: Chaffin
mesh_terms: D000818:Animals; D018955:CD36 Antigens / Q000235:genetics* / Q000378:metabolism; D002478:Cells, Cultured; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D004967:Estrogens / Q000378:metabolism; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects; D006107:Granulosa Cells / Q000187:drug effects* / Q000378:metabolism; D008074:Lipoproteins / Q000494:pharmacology*; D034461:Luteinization / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D008253:Macaca mulatta; D011374:Progesterone / Q000378:metabolism; D011973:Receptors, LDL / Q000235:genetics* / Q000378:metabolism; D013256:Steroids / Q000096:biosynthesis*
chemical_list: D018955:CD36 Antigens; D006063:Chorionic Gonadotropin; D004967:Estrogens; D008074:Lipoproteins; D011973:Receptors, LDL; D013256:Steroids; D011374:Progesterone