Large and small cells of the porcine corpus luteum: Differential capacity to secrete estradiol and aromatize exogenous androgen during mid- and late luteal phase

It has been demonstrated previously that aromatization capacity of luteal cells increased as the luteal phase progresses, suggesting that estradiol secretion by regressing corpora lutea could play an active role in regulation of the estrus cycle. To determine whether a specific luteal subpopulation is responsible for this process, luteal cells collected from mature (8-10 days after ovulation) and regressing (14-16 days after ovulation) corpora lutea were separated at unit gravity into small (14-26 mu m) and large (26-38 mu m) cell types. Aliquots of separated cells were incubated overnight in M199 medium alone (= control) or in medium containing: 10 M(-5) T, 10(-6) M or 10(-7) M T or 0.1 x 10(-3) M, 0.5 x 10(-3) M or 1 x 10(-3) M aromatase inhibitor CGS 16949A. Both cell types were capable of estradiol production without the addition of substrates. The endogenous content of estradiol was always higher in large granulosa-derived luteal cells (LC) than in small theca-derived luteal cells (SC), and was higher in the late (LLP) than in the mid-luteal (MLP) phase. Both types of cells responded to testosterone by increasing estradiol secretion. Adding aromatase inhibitor to LC isolated from MLP and LLP decreased testosterone-stimulated estradiol secretion. On the other hand, aromatase inhibitor had no effect on testosterone-stimulated estradiol secretion by SC isolated during MLP, and inhibited testosterone-stimulated tradiol secretion by SC isolated during LLP. These data are the first to show the ability of both populations of porcine luteal cells to aromatize exogenous testosterone. The observed lack of aromatase inhibitor influence upon basal secretion of estradiol by SC separated from mature corpora lutes, and the decrease of testosterone-stimulated estradiol secretion by SC isolated from regressing corpora lutea, indicate that cytodifferentiation during luteinization could cause expression of P-450 arom in theca-derived luteal cells.