title: [Comparative studies on steroidogenesis and prostaglandins production by luteal cells in newly formed corpora lutea and early pregnancy].
abstract: The present study was undertaken to assess the ability of cultured luteal cells from human corpora lutea (CL) in the mid luteal phase and the early pregnancy to secrete steroids and prostaglandins (PGs). Luteal cells responded to hCG with a significant increase (2- to 4-fold) in progesterone (P) production. The addition of hCG to the culture media did not stimulate estradiol (E2) production. In contrast, both P and E2 secretion by luteal cells in early pregnancy were significantly lower than those found in the mid luteal phase. Exposure to hCG did not affect P production by luteal cells in early pregnancy. Arachidonic acid (AA) significantly stimulated PGE2 synthesis by luteal cells in the mid luteal phase in a dose-dependent manner. Both basal PGE2 production and the responsiveness to AA were maintained for the duration of the culture. However, hCG did not affect AA-stimulated PGE2 production. Both PGF2 alpha and 6-keto-PGF1 alpha production abruptly declined as the culture proceeded. PG synthesis by cultured luteal cells in early pregnancy was significantly lower than in the mid luteal phase. The ultrastructural characteristics of luteal cells in early pregnancy, which contained lipid droplets, granular and agranular endoplasmic reticulum and large spherical mitochondria, were maintained after 10 days in culture. The present results demonstrate that P and PGE2 production by cultured luteal cells predominate during the mid luteal phase. These data suggest that PGE2, but not PGF2 alpha, may be involved in the regulation of CL function in the menstrual cycle.
authors.affiliation: Department of Obstetrics and Gynecology, Fujita-Gakuen Health University School of Medicine, Aichi.
authors.forename: F
authors.initials: F
authors.lastname: Ichikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshimura
authors.forename: T
authors.initials: T
authors.lastname: Ebihara
authors.forename: T
authors.initials: T
authors.lastname: Sawada
authors.forename: S
authors.initials: S
authors.lastname: Kawakami
authors.forename: M
authors.initials: M
authors.lastname: Fukushima
authors.forename: T
authors.initials: T
authors.lastname: Oda
authors.forename: T
authors.initials: T
authors.lastname: Ohno
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000328:Adult; D001095:Arachidonic Acids; D002478:Cells, Cultured; D006063:Chorionic Gonadotropin; D003338:Corpus Luteum / Q000166:cytology / Q000378:metabolism*; D015237:Dinoprost / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D004958:Estradiol / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D008184:Luteal Cells / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D008183:Luteal Phase; D011247:Pregnancy / Q000378:metabolism*; D011261:Pregnancy Trimester, First; D011374:Progesterone / Q000096:biosynthesis*; D011453:Prostaglandins / Q000096:biosynthesis*
chemical_list: D001095:Arachidonic Acids; D006063:Chorionic Gonadotropin; D011453:Prostaglandins; D011374:Progesterone; D004958:Estradiol; D015121:6-Ketoprostaglandin F1 alpha; D015237:Dinoprost; D015232:Dinoprostone