scholarly journals Autophagy Attenuation Hampers Progesterone Synthesis during the Development of Pregnant Corpus Luteum

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 71
Author(s):  
Zonghao Tang ◽  
Zhenghong Zhang ◽  
Hong Zhang ◽  
Yuhua Wang ◽  
Yan Zhang ◽  
...  

The contribution of autophagy to catabolic balance has been well-established in various types of cells, whereas the involvement of autophagy in progesterone synthesis during rat pregnancy still remains unknown. Therefore, the present study was designed to evaluate the role of autophagy in progesterone production during the luteal development of pregnant rats. The results showed autophagy-related proteins was maintained at a low level on day 10 after pregnancy, significantly induced on day 16 and subsided to a relative low level on day 21, which was consistent with the changes of serum progesterone levels. The findings further indicated the contribution of autophagy to progesterone production was regulated by inactivation of Akt/mTOR signaling during the luteal development of pregnant rats in in vivo and in vitro experiments. Further investigations revealed autophagy may be involved in the surge of progesterone production in pregnant rats, as inhibition of autophagy by 3-MA compromised serum progesterone levels. Furthermore, 3-MA treatment also leveled down the number of lipid droplets in luteal cells, implying that autophagy may affect the production of progesterone by manipulating the formation of lipid droplets in luteal cells. In addition, the results suggested that mitophagy was mobilized during the primary stage of luteolysis and inhibition of autophagy promoted the increase of redundant mitochondrial and cytoplasmic cytochrome C in luteal cells of pregnant rats. Taken together, the present study indicated that autophagy-related proteins were induced by the inactivation of Akt/mTOR signaling and then contributed to the progesterone production possibly by affecting the formation of intracellular lipid droplets during the luteal development of pregnant rats. To our knowledge, this will provide a new insight into the important mechanism of autophagy regulating progesterone production in ovaries of pregnant mammals.

1987 ◽  
Vol 40 (3) ◽  
pp. 331 ◽  
Author(s):  
William Hansel ◽  
Hector W Alila ◽  
Joseph P Dowd ◽  
Xiangzhong Yang

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.


2019 ◽  
Vol 102 (2) ◽  
pp. 511-520
Author(s):  
Yanrong Kuai ◽  
Xiaobo Gao ◽  
Huixia Yang ◽  
Haiyan Luo ◽  
Yang Xu ◽  
...  

Abstract Pentachloronitrobenzene (PCNB) is an organochlorine fungicide widely used for crop production and has become an environmental concern. Little is known about the effect of PCNB on ovarian steroidogenesis and follicular development. We found that PCNB stimulated Star expression and progesterone production in cultured rat granulosa cells in a dose-dependent manner. PCNB activated mitogen-activated protein kinase (MAPK3/1) extracellulat regulated kinase (ERK1/2), thus inhibition of either protein kinase A (PKA) or MAPK3/1 signaling pathway significantly attenuated progesterone biosynthesis caused by PCNB, suggesting that PCNB induced progesterone production by activating the cyclic adenosine monophosphate (cAMP/PKA) and MAPK3/1 signaling pathways. Further investigation demonstrated that PCNB induced Star expression and altered MAPK3/1 signaling in ovary tissues of immature SD rats treated with PCNB at the dose of 100, 200, or 300 mg/kg by daily gavage for 7 days, while serum progesterone level was dose-dependently decreased. We demonstrated that PCNB exposure accelerated the recruitment of primordial follicles into the growing follicle pool in ovary tissues, accompanied by increased levels of anti-Mullerian hormone (AMH) in both ovary tissues and serum. Taken together, our data demonstrate for the first time that PCNB stimulated Star expression, altered MAPK3/1 signaling and progesterone production in vivo and in vitro, and accelerated follicular development with a concomitant increase in AMH in ovary tissues and serum. Our findings provide novel insight into the toxicity of PCNB to animal ovary function.


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Xiaolu Qu ◽  
Leyan Yan ◽  
Rihong Guo ◽  
Hui Li ◽  
Zhendan Shi

LPS is a major endotoxin produced by gram-negative bacteria, and exposure to it commonly occurs in animal husbandry. Previous studies have shown that LPS infection disturbs steroidogenesis, including progesterone production, and subsequently decreases animal reproductive performance. However, little information about the underlying mechanisms is available thus far. In the present study, an in vitro-luteinized porcine granulosa cell model was used to study the underlying molecular mechanisms of LPS treatment. We found that LPS significantly inhibits progesterone production and downregulates the expressions of progesterone synthesis-associated genes (StAR, CYP11A1, and 3β-HSD). Furthermore, the levels of ROS were significantly increased in an LPS dose-dependent manner. Moreover, transcriptional factors GATA4 and GATA6, but not NR5A1, were significantly downregulated. Elimination of LPS-stimulated ROS by melatonin or vitamin C could restore the expressions of GATA4, GATA6, and StAR. In parallel, StAR expression was also inhibited by the knockdown of GATA4 and GATA6. Based on these data, we conclude that LPS impairs StAR expression via the ROS-induced downregulation of GATA4 and GATA6. Collectively, these findings provide new insights into the understanding of reproductive losses in animals suffering from bacterial infection and LPS exposure.


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

Reproduction ◽  
1984 ◽  
Vol 72 (1) ◽  
pp. 137-141 ◽  
Author(s):  
A. K. Mukhopadhyay ◽  
A. Kumar ◽  
R. Tams ◽  
H. G. Bohnet ◽  
F. A. Leidenberger

1983 ◽  
Vol 96 (3) ◽  
pp. 499-503 ◽  
Author(s):  
G. J. S. Tan ◽  
J. S. G. Biggs

The effects of prolactin on steroidogenesis were studied in dispersed luteal cells prepared from human corpora lutea of the menstrual cycle. Prolactin, at concentrations of 0·1–1000 ng/ml, had no effect on progesterone production by luteal cells during short-term incubation (3 h). However, in two out of five corpora lutea, higher concentrations of prolactin (100 and 1000 ng/ml) significantly reduced the oestradiol-17β production induced by human chorionic gonadotrophin (hCG; 10 i.u./ml); lower doses of prolactin had little effect. In the remaining corpora lutea, prolactin failed to affect either basal or hCG-induced production of oestradiol-17β. These results are discussed in relation to the mechanism by which prolactin influences human ovarian function.


2017 ◽  
Vol 29 (1) ◽  
pp. 137
Author(s):  
F. C. Destro ◽  
I. Martin ◽  
F. D. C. Landim-Alvarenga ◽  
R. Sartori Filho ◽  
J. L. Pate ◽  
...  

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.


1986 ◽  
Vol 64 (12) ◽  
pp. 1556-1560
Author(s):  
D. W. Beckner ◽  
J. G. Manns

The objectives of this study were the following: (i) to determine if ovine conceptus secretory products are directly luteotrophic to luteal tissue in vitro and (ii) to determine if ovine conceptus secretory products stimulate endometrial tissue to secrete a luteotropin in vitro. Conceptus-conditioned medium (CCM) was prepared by incubating day 14 ovine conceptuses in minimal essential medium (MEM) for 24 h and harvesting the supernatant. Endometrium-conditioned CCM (E-CCM) and endometrium-conditioned medium (ECM) were prepared by incubating dispersed ovine endometrial cells from day 9–10 cycling ewes in CCM or MEM, respectively, for 16 h and harvesting the supernatants. Media, conditioned as described, were incubated at various dilutions with dispersed luteal cells from day 9–10 cycling ewes for 90 min or 6 h in the absence or presence of 50 ng/mL ovine luteinizing hormone (oLH). CCM did not alter progesterone (P4) production in the 90-min incubation but did increase (p < 0.05) P4 production in the 6-h incubation (1:4, 1:8, 1:16 dilutions). When coincubated with oLH, CCM did not increase P4 production above that stimulated by oLH alone. The effect of E-CCM was similar to CCM or ECM and did not differ significantly from basal. It is concluded that the day 14 ovine conceptus does secrete a factor that is able to directly stimulate P4 secretion by luteal cells in a 6-h, but not a 90-min, incubation. Conceptus secretory products did not stimulate endometrial cells to secrete a luteotropin. The data are consistent with the suggestion that the luteotrophic factor secreted by the conceptus is a prostaglandin of the E series.


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