摘要:

not available

ISSN:0008-4212    

DOI:10.1139/y85-044

出版商:NRC Research Press    

年代:1985

数据来源: NRC

摘要:

Ovine luteal tissue contains two distinct steroidogenic cell types, small (8–20 μm) and large (>20 μm), which differ based on morphological and biochemical criteria. Unstimulated small cells secrete low levels of progesterone, respond to LH or dibutyryl cAMP (dbcAMP) with enhanced secretion of progesterone, and contain most of the receptors for LH. The unstimulated large cells, conversely, secrete high levels of progesterone, have few, if any, receptors for LH, and do not respond to LH –or dbcAMP with increased progesterone secretion. The lack of response to dbcAMP by large cells was investigated. Large cells incubated in the presence of cholesterol, ram serum, or 25-hydroxycholesterol did not demonstrate substrate limitation. Hormone-independent stimulation of adenylate cyclase by cholera toxin or forskolin resulted in increased adenylate cyclase activities (P < 0.01), cAMP accumulation (P < 0.05), and the binding of endogenous cAMP (P < 0.05) by type 1 cAMP-dependent protein kinase in both small and large cells. These treatments were accompanied by enhanced secretion of progesterone (P < 0.05) in small cells. In contrast, large cells did not respond with an increase in progesterone secretion under these conditions. These observations suggest that the high rate of secretion of progesterone in unstimulated large cells is not regulated by cAMP.

ISSN:0008-4212    

DOI:10.1139/y85-045

出版商:NRC Research Press    

年代:1985

数据来源: NRC

摘要:

Both gonadotropin-releasing hormone (GnRH) and prostaglandin F2α (PGF2α) can inhibit cAMP and progesterone production in the corpus luteum; however, their mechanism of action is not known. GnRH or PGF2α causes a rapid and marked increase of labelling of phosphatidylinositol (PI) and phosphatidic acid (PA) in rat luteal cells in culture. The incorporation of radioactivity is increased as early as 2 and 5 min into PA and PI, respectively. The labelling of the other phospholipids is not affected. GnRH and PGF2α exert their stimulatory effects on PA–PI turnover at a mean effective dose value of ca. 15 and 100 nM, respectively. Their effects appeared to be additive when both agents were present in the same incubations. Interestingly, addition of the calcium ionophore A23187 also causes a dramatic increase of PA–PI turnover in luteal cells. By contrast, human chorionic gonadotropin and isoproterenol, agents that stimulate cAMP and progesterone production in luteal cells, as well as PGE2(1 μM), all fail to alter phospholipid labelling; dibutyryl or 8-bromo-cAMP (2–5 mM) actually attentuates the GnRH or PGF2αeffect on PI and PA. A very similar PA–PI response to GnRH and PGF2α has also been observed using rat granulosa cells in culture. It seems that following their binding to membrane receptors, GnRH and PGF2α may share a common mechanism in the ovarian cell, possibly involving the stimulation of PA–PI metabolism.

ISSN:0008-4212    

DOI:10.1139/y85-046

出版商:NRC Research Press    

年代:1985

数据来源: NRC

摘要:

This review summarizes evidence suggesting a direct luteotrophic role for the hypophyseal hormone prolactin (PRL). This direct role consists of the capability to stimulate progesterone synthesis in vitro, the capability to maintain the membrane fluidity and receptors for luteinizing hormone and the capability to import substrate for progesterone synthesis. The time required for PRL-induced luteotrophic events is in the order of hours and sometimes days, and it appears that the effects are not associated with acute intracellular changes. The relatively slow responses and the stimulation of specific protein synthesis by PRL in target tissues other than the ovary suggest that PRL may function primarily through activation of the genome. PRL may induce the synthesis of specific luteal proteins, including enzymes for the regulation of intracellular substrate pools, membrane receptors for LH, or receptor proteins for lipoproteins, a major extracellular source of substrate.

ISSN:0008-4212    

DOI:10.1139/y85-047

出版商:NRC Research Press    

年代:1985

数据来源: NRC

摘要:

Administration of human chorionic gonadotropin (hCG) to pregnant mare's serum gonadotropin – hCG primed rats results in the loss ofin vitroresponsiveness of the ovaries to exogenous gonadotropins for progesterone production. This state is associated with a loss of membrane receptors for hCG and a concomitant increase in lipoprotein receptors. Although lipoproteins potentiated gonadotropin response in ovaries from saline-injected rats, no stimulation was observed in hCG-desensitized ovarian cells. Examination of the time course for the loss of lipoprotein response after hCG injection revealed that injection with 50 IU of hCG results in a loss of gonadotropin response as early as 1 h after injection, but exogenous cholesterol-carrying lipoprotein fractions, LDL and HDL, were capable of stimulating progesterone production up to 4 h after hormone injection. Measurement of endogenous cholesteryl ester content showed that there was a 72% decline during this period with a concomitant increase in the basal progesterone production. One hour after hCG injection there was no stimulation of steroidogenesis by hCG in the presence or absence of exogenous lipoproteins. The refractoriness to exogenous hCG appeared only 4 h later when the hCG dose was reduced to 10 IU, whereas with 25 IU of hCG, the effect was similar to that observed using 50 IU of hCG. Such diverse steroidogenic stimuli as hCG, LH, LDL, cAMP, and cholera enterotoxin failed to stimulate progesterone synthesisin vitroin luteal cells of rats injected with 50 IU of hCG 48 h prior to sacrifice. Cellular uptake of reconstituted LDL bearing [3H]cholesterol linoleate was increased twofold in hCG-desensitized rat ovarian cells, whereas incorporation of [3H]cholesterol into progesterone from this reconstituted LDL was not stimulated by exogenous hCG. Examination of the binding of [125I]iodoLDL and [125I]iodoHDL to isolated plasma membrane from luteal cells showed that the binding of both these lipoproteins was increased twofold within 12 h after hCG injection, but returned to control levels by 72 h. From these results it is concluded that during hCG-induced loss of progesterone production in the ovary, the cells are fully capable of binding and transporting exogenously supplied plasma lipoprotein tractions. The steroidogenic lesion arises from the loss of hCG receptor mediated responsive system, but is not related to loss of the substrate pool needed for steroidogenesis.

ISSN:0008-4212    

DOI:10.1139/y85-048

出版商:NRC Research Press    

年代:1985

数据来源: NRC