DEVELOPMENTAL-STUDY ON CAPACITY OF RABBIT GRANULOSA-CELLS TO RESPOND TO TROPHIC HORMONES AND SECRETE PROGESTERONE INVITRO
DEVELOPMENTAL-STUDY ON CAPACITY OF RABBIT GRANULOSA-CELLS TO RESPOND TO TROPHIC HORMONES AND SECRETE PROGESTERONE INVITRO
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DOI:
10.1016/0012-1606(74)90124-9
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发表时间:
1974-01-01
影响因子:
2.7
通讯作者:
RYAN, KJ
中科院分区:
文献类型:
--
作者:
ERICKSON, GF;CHALLIS, JRG;RYAN, KJ
To determine when undifferentiated rabbit granulosa cells first develop the capacity to secrete progesterone, pieces of intact ovaries from neonatal rabbits (newborn—30 days old) and pure granulosa cells from 150–1200 μm follicles at 60–600 days old were cultured in vitro for 6–10 days with human chorionic gonadotropin (HCG), Pergonal (LH FSH), dibutyryl cyslic AMP (Bu 2 CAMP), prostaglandin E 2, estradiol-17β, and as controls. The culture medium was collected every 2 days, and progesterone, estrone, and estradiol-17β were measured by radioimmunoassay. None of the neonatal ovaries or granulosa cell cultures secreted estrone or estradiol-17β spontaneously or in response to stimulation by gonadotropins, Bu 2 CAMP, or prostaglandin E 2. Control cultures of newborn and 7-day-old ovaries did not secrete progesterone, but ovaries from 17-and 30-day-old rabbits did. Gonadotropins and Bu 2 CAMP induced progesterone secretion in 7-day-old ovaries and stimulated its production 5-10-fold in ovaries at 17 and 30 days old, but prostaglandin E 2 and estradiol-17β were without effect. Granulosa cells from all antral follicles (200–1200 μm) secreted progesterone spontaneously, and its production was stimulated 100–1000-fold with gonadotropins and Bu 2 CAMP, but not with estradiol-17β or prostaglandin E 2. In contrast, granulosa cells from 100–150 μm preantral follicles from 200-day-old animals did not secrete progesterone under these culture conditions. These results demonstrate that rabbit granulosa cells differentiate the capacity to secrete progesterone at the time the primary follicle develops an antrum, and suggest the differentiation process involves the acquisition of the capacity to respond to gonadotropins perhaps by the synthesis or unmasking of gonadotropin receptors.