A POSSIBLE INTERRELATIONSHIP BETWEEN GONADOTROPHIN STIMULATION AND PROSTAGLANDIN F2α INHIBITION OF STEROIDOGENESIS BY GRANULOSA-LUTEAL CELLS IN VITRO

1977 ◽  
Vol 73 (1) ◽  
pp. 71-78 ◽  
Author(s):  
K. M. HENDERSON ◽  
K. P. McNATTY
Keyword(s):  
Tissue Culture ◽  
Corpus Luteum ◽  
Prostaglandin F2α ◽  
Luteal Cell ◽  
Luteal Cells ◽  
Lytic Action ◽  
Progesterone Production ◽  
Prostaglandin F

SUMMARY The newly formed corpus luteum of many species is refractory to the lytic action of prostaglandin F2α (PGF2α). This phenomenon was studied utilizing porcine, bovine and human granulosa-luteal cells in tissue culture. The steroidogenic potential of the granulosa-luteal cells was critical in determining whether PGF2α could inhibit progesterone production. Since the steroidogenic potential of the granulosa-luteal cell is related to the amount of LH bound to the cell, the bound LH may protect the granulosa-luteal cells from the lytic action of PGF2α. Finally, a 'see-saw' type of interaction between LH and PGF2α is postulated to account for the resistance of the newly formed corpus luteum to PGF2α

scholarly journals Estrogen promotes luteolysis by redistributing prostaglandin F2α receptors within primate luteal cells

Reproduction ◽  
2015 ◽  
Vol 149 (5) ◽  
pp. 453-464 ◽  
Author(s):  
Soon Ok Kim ◽  
Nune Markosyan ◽  
Gerald J Pepe ◽  
Diane M Duffy
Keyword(s):  
Estrogen Receptor ◽  
Granulosa Cells ◽  
Prostaglandin F2α ◽  
Luteal Cell ◽  
Corpora Lutea ◽  
Dependent Manner ◽  
Perinuclear Region ◽  
Luteal Cells ◽  
Progesterone Production

Prostaglandin F2α (PGF2α) has been proposed as a functional luteolysin in primates. However, administration of PGF2α or prostaglandin synthesis inhibitors in vivo both initiate luteolysis. These contradictory findings may reflect changes in PGF2α receptors (PTGFRs) or responsiveness to PGF2α at a critical point during the life span of the corpus luteum. The current study addressed this question using ovarian cells and tissues from female cynomolgus monkeys and luteinizing granulosa cells from healthy women undergoing follicle aspiration. PTGFRs were present in the cytoplasm of monkey granulosa cells, while PTGFRs were localized in the perinuclear region of large, granulosa-derived monkey luteal cells by mid-late luteal phase. A PTGFR agonist decreased progesterone production in luteal cells obtained at mid-late and late luteal phases, but did not decrease progesterone production by granulosa cells or luteal cells from younger corpora lutea. These findings are consistent with a role for perinuclear PTGFRs in functional luteolysis. This concept was explored using human luteinizing granulosa cells maintained in vitro as a model for luteal cell differentiation. In these cells, PTGFRs relocated from the cytoplasm to the perinuclear area in an estrogen- and estrogen receptor-dependent manner. Similar to our findings with monkey luteal cells, human luteinizing granulosa cells with perinuclear PTGFRs responded to a PTGFR agonist with decreased progesterone production. These data support the concept that PTGFR stimulation promotes functional luteolysis only when PTGFRs are located in the perinuclear region. Estrogen receptor-mediated relocation of PTGFRs within luteal cells may be a necessary step in the initiation of luteolysis in primates.

scholarly journals HIF-1α Activation Promotes Luteolysis by Enhancing ROS Levels in the Corpus Luteum of Pseudopregnant Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zonghao Tang ◽  
Jiajie Chen ◽  
Zhenghong Zhang ◽  
Jingjing Bi ◽  
Renfeng Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Corpus Luteum ◽  
Cell Apoptosis ◽  
In Vitro Study ◽  
Luteal Cell ◽  
Independent Manner ◽  
Luteal Regression ◽  
Luteal Cells

The increase of oxidative stress is one of the important characteristics of mammalian luteal regression. Previous investigations have revealed the essential role of reactive oxygen species (ROS) in luteal cell death during luteolysis, while it is unknown how ROS is regulated in this process. Considering the decrease of blood flow and increase of PGF2α during luteolysis, we hypothesized that the HIF-1α pathway may be involved in the regulation of ROS in the luteal cell of the late corpus luteum (CL). Here, by using a pseudopregnant rat model, we showed that the level of both HIF-1α and its downstream BNIP3 was increased during luteal regression. Consistently, we observed the increase of autophagy level during luteolysis, which is regulated in a Beclin1-independent manner. Comparing with early (Day 7 of pseudopregnancy) and middle CL (Day 14), the level of ROS was significantly increased in late CL, indicating the contribution of oxidative stress in luteolysis. Inhibition of HIF-1α by echinomycin (Ech), a potent HIF-1α inhibitor, ameliorated the upregulation of BNIP3 and NIX, as well as the induction of autophagy and the accumulation of ROS in luteal cells on Day 21 of pseudopregnancy. Morphologically, Ech treatment delayed the atrophy of the luteal structure at the late-luteal stage. An in vitro study indicated that inhibition of HIF-1α can also attenuate PGF2α-induced ROS and luteal cell apoptosis. Furthermore, the decrease of cell apoptosis can also be observed by ROS inhibition under PGF2α treatment. Taken together, our results indicated that HIF-1α signaling is involved in the regression of CL by modulating ROS production via orchestrating autophagy. Inhibition of HIF-1α could obviously hamper the apoptosis of luteal cells and the process of luteal regression.

scholarly journals Control of Steroidogenesis in Small and Large Bovine Luteal. Cells

1987 ◽  
Vol 40 (3) ◽  
pp. 331 ◽  
Author(s):  
William Hansel ◽  
Hector W Alila ◽  
Joseph P Dowd ◽  
Xiangzhong Yang
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Corpus Luteum ◽  
Luteal Cell ◽  
Lipoxygenase Pathway ◽  
Luteal Cells ◽  
Kinase C ◽  
Bovine Corpus Luteum ◽  
Progesterone Synthesis

Evidence was cited to show that: (1) prostacyclin (PGI2) plays a luteotrophic role in the bovine corpus luteum and that products of the lipoxygenase pathway of arachidonic acid metabolism, especially 5-hydroxyeicosatetraenoic acid play luteolytic roles; (2) oxytocin of luteal cell origin plays a role in development, and possibly in regression, of the bovine corpus luteum; and (3) luteal cells arise from two sources; the characteristic small luteal cells at all stages of the o~strous cycle and pregnancy are of theca cell origin; the large cells are of granulosa cell origin early in the cycle, but a population of theca-derived large cells appears later in the cycle. Results of in vitro studies with total dispersed cells and essentially pure preparations of large and small luteal cells indicate that : (1) the recently described Ca2+ -polyphosphoinositol-protein kinase C second messenger system is involved in progesterone synthesis in the bovine corpus luteum; (2) activation of protein kinase C is stimulatory to progesterone synthesis in the small luteal cells; (3) activation of protein kinase C has no effect on progesterone synthesis in the large luteal cells; and (4) protein kinase C exerts its luteotrophic effect in total cell preparations, in part at least, by stimulating the production of prostacyclin. The protein kinase C system may cause down regulation of LH receptors in the large cells.

In. vitro evaluation of corpus luteum function of cycling and pregnant rhesus monkeys: Progesterone production by dispersed luteal cells

Steroids ◽  
1976 ◽  
Vol 27 (4) ◽  
pp. 543-551 ◽  
Author(s):  
Richard L. Stouffer ◽  
Wilbert E. Nixon ◽  
Bela J. Gulyas ◽  
David.K. Johnson ◽  
Gary D. Hodgen
Keyword(s):  
Corpus Luteum ◽  
Rhesus Monkeys ◽  
In Vitro Evaluation ◽  
Luteal Cells ◽  
Progesterone Production

Ovarian production of progesterone and 20α-dihydroprogesterone in vitro following prostaglandin F2α induced luteolysis in the superluteinized rat

1984 ◽  
Vol 105 (2) ◽  
pp. 258-265 ◽  
Author(s):  
P. A. Torjesen ◽  
A. Aakvaag
Keyword(s):  
Adenylyl Cyclase ◽  
Prostaglandin F2α ◽  
Mitochondrial Fraction ◽  
Supernatant Fraction ◽  
Production Rates ◽  
Cyclic Monophosphate ◽  
Progesterone Production ◽  
Progesterone Secretion ◽  
Prostaglandin F

Abstract. Superluteinized rats were injected with the prostaglandin F2α (PGF2α) analogue cloprostenol to induce luteolysis. The treatment decreased progesterone production of ovarian homogenates from 8.9 ± 0.5 to 4.0 ± 0.7 nmol/ovary/10 min (mean ± sem) within 40 min. tochondrial fractions isolated from control and cloprostenol treated animals produced 4.7 ± 0.4 and 2.8 ± 0.3 nmol progesterone/ovary/10 min, respectively. Thus, the PGF2α analogue treatment significantly reduced mitochondrial progesterone production. Addition of the 15 000 × g supernatant fraction did not influence the progesterone production rates of the mitochondrial fraction. The basal progesterone secretion from quartered ovaries decreased from 1.50 ± 0.15 to 0.38 ± 0.05 nmol/ovary during the initial 15 min of incubation following cloprostenol administration. hCG and N6,O2'-dibutyryladenosine 3':5'-cyclic monophosphate (DBC) stimulated the progesterone secretion from quartered ovaries, but the response was delayed in ovaries obtained from cloprostenol treated animals. Although the response was delayed, the progesterone secretion following cloprostenol treatment was re-activated with cAMP either directly or via hCG. The increment in progesterone secretion above unstimulated controls in response to DBC was not influenced by the cloprostenol treatment while the increment caused by hCG was decreased. Our data suggest that: 1) PGF2α deactivates mitochondrial progesterone production, 2) this deactivation may be overcome by cAMP, and 3) PGF2α decreases gonadotrophin responsive adenylyl cyclase.

60 EFFECTS OF CONCANAVALIN A ON THE PROGESTERONE PRODUCTION BY BOVINE STEROIDOGENIC LUTEAL CELLS IN VITRO

2017 ◽  
Vol 29 (1) ◽  
pp. 137
Author(s):  
F. C. Destro ◽  
I. Martin ◽  
F. D. C. Landim-Alvarenga ◽  
R. Sartori Filho ◽  
J. L. Pate ◽  
...  
Keyword(s):  
Concanavalin A ◽  
Culture Media ◽  
Prostaglandin F2α ◽  
Inhibitory Effect ◽  
Humid Atmosphere ◽  
Luteal Cells ◽  
Progesterone Production ◽  
Fetal Bovine ◽  
Culture Differences

The corpus luteum is a temporary organ that is responsible for progesterone (P4) secretion and is essential for the establishment and maintenance of pregnancy in cattle. Concanavalin A (CONA) is a lectin that was originally extracted from the Jack bean (Canavalia ensiformis) and that interacts with several kinds of cells, including immune cells and luteal cells. The aim of the present study was to evaluate the effects of CONA on the P4 production by bovine steroidogenic luteal cells (LC) in vitro. Luteal cells were collected during the mid-luteal stage (at 10–12 days following ovulation) and processed in the laboratory. Luteal cells were grown for 7 days in a humid atmosphere with 5% CO2, with or without 10% fetal bovine serum (FBS), and were subjected to the following treatments: control: no treatment; CONA (10 μg mL−1); LH (100 μg mL−1); CONA+LH; LH (100 μg mL−1) + prostaglandin F2α (PGF2α; 10 ng mL−1); CONA+LH+PGF2α. Samples of the culture media were collected on Day 1 and Day 7 for P4 quantification. The cells were counted on Day 7 of culture. Differences between treatments were considered statistically significant at P < 0.05. The P4 concentration in the culture media was numerically greater on Day 1 (558.0 ng mL−1) than on Day 7 (25.4 ng mL−1). The P4 concentration in the culture media was numerically greater for treatments with 10% FBS than for the FBS-free treatments, and the presence of CONA decreased LC P4-secreting capacity. This effect required more than 24 h of exposure to CONA to be fully manifested. On Day 1 of culture, CONA had no effect on P4 production of LC cultured in serum-free medium (P > 0.05).The suppressive action of CONA was more pronounced for cultures without FBS. By Day 7 of culture, the effects of CONA on P4 production were readily apparent. In the absence of serum, CONA had a highly significant (P < 0.01) inhibitory effect on basal progesterone production, as well as in the presence of LH or LH + PGF. In the presence of FBS, there was a tendency for decreased P4 in response to CONA in the LH- and the LH + PGF-treated cells (P = 0.090 and 0.085, respectively). The number of the cells present on Day 7 was not affected by the treatments tested (P > 0.05). More studies are required to better understand the effect of CONA on the P4 production of bovine LC. Financial support from FAPESP is acknowledged: grant no. 2013/00992–3, grant no. 2013/07439–8, and grant no. 2015/01940–2.

scholarly journals Cell death induced by serum deprivation in luteal cells involves the intrinsic pathway of apoptosis

Reproduction ◽  
2006 ◽  
Vol 131 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Alicia A Goyeneche ◽  
Jacquelyn M Harmon ◽  
Carlos M Telleria
Keyword(s):  
Cell Death ◽  
Corpus Luteum ◽  
Simian Virus 40 ◽  
Full Length ◽  
Luteal Cell ◽  
Serum Starvation ◽  
Endocrine Gland ◽  
Luteal Cells ◽  
Defined Culture

The corpus luteum is a transient endocrine gland specializing in the production of progesterone. The regression of the corpus luteum involves an abrupt decline in its capacity for producing progesterone followed by its structural involution, which is associated with apoptosis of the luteal cells. An in vitro experimental approach is needed to study the molecular mechanisms underlying hormonal regulation of luteal cell death under defined experimental conditions. In this study, we investigated simian virus-40-transformed luteal cells to determine whether they can be driven to apoptosis and, if so, to define the intracellular pathway involved. Luteal cells were cultured in the presence or absence of fetal bovine serum for 24 or 48 h. Under serum starvation conditions, the luteal cells underwent growth arrest accompanied by cell death as evaluated by dye exclusion, and confirmed by two-color fluorescence cell viability/cytotoxicity assay. We next studied whether serum starvation-induced death of luteal cells occurred by apoptosis. Morphologic features of apoptosis were observed in cells stained with hematoxylin after being subjected to serum starvation for 48 h. The apoptotic nature was further confirmed by in situ 3′-end labeling and fragmentation of genomic DNA. Apoptosis of serum-deprived luteal cells was dependent upon caspase activation. Serum starvation induced cleavage of poly (ADP-ribose) polymerase (PARP), suggesting that caspase-3 had been activated under the stress of withdrawal of growth factors. This was confirmed by cleavage of full-length procaspase-3. Finally, the fact that serum starvation promoted the cleavage of full-length procaspase-9 and the decrease in the expression of endogenous Bid, a BH-3-only proapoptotic protein of the Bcl-2 family, indicates that the intrinsic (i.e., mitochondrial) pathway of apoptosis was activated. In summary, we have characterized an in vitro experimental model of luteal cell death that can be utilized to evaluate the role of hormones in apoptosis of luteal cells under defined culture conditions, and to study the mechanism of luteal regression.

Human growth hormone enhances progesterone production by human luteal cells in vitro. II. Evidence of a distinct effect on two luteal cell types

1993 ◽  
Vol 60 (1) ◽  
pp. 47-52 ◽  
Author(s):  
Nicoletta Di Simone ◽  
Roberta Castellani ◽  
Antonio Lanzone ◽  
Alessandro Caruso ◽  
Salvatore Mancuso
Keyword(s):  
Growth Hormone ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Cell Types ◽  
Luteal Cell ◽  
Luteal Cells ◽  
Distinct Effect ◽  
Progesterone Production

INFLUENCE OF 16-ARYLOXYPROSTAGLANDINS ON THE PRODUCTION OF PROGESTERONE BY HUMAN GRANULOSA CELLS IN VITRO

1976 ◽  
Vol 71 (2) ◽  
pp. 259-263 ◽  
Author(s):  
K. M. HENDERSON
Keyword(s):  
Tissue Culture ◽  
Adenylate Cyclase ◽  
Granulosa Cells ◽  
Farm Animals ◽  
Human Granulosa Cells ◽  
Progesterone Production ◽  
Porcine Granulosa Cells ◽  
Prostaglandin F

SUMMARY 16-Aryloxy analogues of prostaglandin F2α(PGF2α) are potent luteolysins in laboratory and farm animals. When their effect on progesterone production by luteinized human granulosa cells in tissue culture was investigated inhibition of both basal and gonadotrophin-stimulated progesterone production was observed, so revealing characteristics expected of potential human luteolysins. The analogues were, however, unable to inhibit progesterone production stimulated by PGE2, suggesting that like PGF2α these compounds may act by specifically blocking LH-activated adenylate cyclase. The 16-aryloxyprostaglandins similarly inhibited progesterone production by porcine granulosa cells, so that the effects observed with the 16-aryloxyprostaglandins in vitro may be indicative of their potential in vivo.

Prostaglandin F2α- and phorbol 12-myristate-13-acetate-stimulated progesterone production by cultured human luteal cells in the mid-luteal phase: prostaglandin F2α increases cytosolic Ca2+ and inositol phosphates

1992 ◽  
Vol 133 (3) ◽  
pp. 451-458 ◽  
Author(s):  
T. Endo ◽  
H. Watanabe ◽  
H. Yamamoto ◽  
S. Tanaka ◽  
M. Hashimoto
Keyword(s):  
Luteal Phase ◽  
Inositol Phosphates ◽  
Prostaglandin F2α ◽  
Free Calcium ◽  
Corpora Lutea ◽  
Luteal Cells ◽  
Progesterone Production ◽  
Kinase C ◽  
Prostaglandin F ◽  
Human Corpus Luteum

ABSTRACT While prostaglandin F2α (PGF2α) has been thought to be a natural luteolysin in non-primates, a luteolytic effect in the human corpus luteum is less evident. We therefore investigated the action of PGF2α on monolayer cultures of human luteal cells obtained from mid-luteal phase corpora lutea. PGF2α increased basal and human chorionic gonadotrophin (hCG)-stimulated progesterone production by human cultured luteal cells. A potent tumour-promoting phorbol ester, phorbol 12-myristate-13-acetate (PMA), also stimulated progesterone production by cultured human luteal cells. Although human luteal cells were incubated for 24 h with PMA, hCG was still able to stimulate the production of progesterone by PMA-pretreated cells. However, PMA pretreatment blocked the ability of PGF2α to stimulate progesterone production. It is possible that the luteotrophic effect of PGF2α may be mediated, in part, by the activation of protein kinase C. Addition of PGF2α to suspensions of human luteal cells preincubated with myo-[2-3H]inositol promoted an increase in labelled inositol phosphates. PGF2α also rapidly increased intracellular free Ca2+ in human luteal cells loaded with the fluorescent Ca2+ probe, fura-2. We conclude that PGF2α and PMA stimulate progesterone production and that PGF2α increases the intracellular free calcium and inositol phosphates of human cultured luteal cells in the mid-luteal phase. Journal of Endocrinology (1992) 133, 451–458

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