scholarly journals Estrogenic Compounds Impair Primordial Follicle Formation by Inhibiting the Expression of Proapoptotic Hrk in Neonatal Rat Ovary

2016 ◽  
Vol 95 (4) ◽  
pp. 78-78 ◽  
Author(s):  
H. Zhang ◽  
K. Nagaoka ◽  
K. Usuda ◽  
K. Nozawa ◽  
K. Taya ◽  
...  
Keyword(s):  
Primordial Follicle ◽  
Neonatal Rat ◽  
Estrogenic Compounds ◽  
Rat Ovary

scholarly journals Phosphodiesterases in the rat ovary: effect of cAMP in primordial follicles

Reproduction ◽  
2015 ◽  
Vol 150 (1) ◽  
pp. 11-20 ◽  
Author(s):  
Tonny Studsgaard Petersen ◽  
Martin Stahlhut ◽  
Claus Yding Andersen
Keyword(s):  
Primordial Follicle ◽  
Neonatal Rat ◽  
Intracellular Camp ◽  
Corpora Lutea ◽  
Dependent Manner ◽  
Primordial Follicles ◽  
Primordial Follicle Activation ◽  
Rat Ovary ◽  
Follicle Differentiation ◽  
Follicle Activation

Phosphodiesterases (PDEs) are important regulators of the intracellular cAMP concentration, which is a central second messenger that affects a multitude of intracellular functions. In the ovaries, cAMP exerts diverse functions, including regulation of ovulation and it has been suggested that augmented cAMP levels stimulate primordial follicle growth. The present study examined the gene expression, enzyme activity and immunolocalization of the different cAMP hydrolysing PDEs families in the rat ovary. Further, the effect of PDE4 inhibition on primordial follicle activation in cultured neonatal rat ovaries was also evaluated. We found varied expression of all eight families in the ovary with Pde7b and Pde8a having the highest expression each accounting for more than 20% of the total PDE mRNA. PDE4 accounted for 15–26% of the total PDE activity. Immunoreactive PDE11A was found in the oocytes and PDE2A in the corpora lutea. Incubating neonatal rat ovaries with PDE4 inhibitors did not increase primordial follicle activation or change the expression of the developing follicle markers Gdf9, Amh, Inha, the proliferation marker Mki67 or the primordial follicle marker Tmeff2. In addition, the cAMP analogue 8-bromo-cAMP did not increase AKT1 or FOXO3A phosphorylation associated with follicle activation or increase the expression of Kitlg known to be associated with follicle differentiation but did increase the Tmeff2, Mki67 and Inha expression in a dose-dependent manner. In conclusion, this study shows that both Pde7b and Pde8a are highly expressed in the rodent ovary and that PDE4 inhibition does not cause an increase in primordial follicle activation.

scholarly journals ESR2 regulates indian hedgehog signaling in neonatal rat ovary

2021 ◽  
Author(s):  
Iman Dilower ◽  
Veera Raghavulu Praveen Chakravarthi ◽  
Eun B Lee ◽  
Subhra Ghosh ◽  
Shaon Borosha ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Hedgehog Signaling ◽  
Primordial Follicle ◽  
Neonatal Rat ◽  
Regulatory Function ◽  
Indian Hedgehog ◽  
Rna Seq ◽  
Transcriptional Regulatory ◽  
Primordial Follicle Activation ◽  
Rat Ovary

The transcriptional regulatory function of estrogen receptor β (ESR2) is essential for the regulation of primordial follicle activation (PFA). Increased PFA due to the loss of ESR2 becomes evident as early as postnatal day 8 (PND8). To identify the ESR2-regulated genes that control PFA, we performed RNA-seq analyses of wildtype, and Esr2 knockout (Esr2KO) neonatal rat ovaries collected on PND4, PND6, and PND8. Among the differentially expressed genes in Esr2KO ovaries, indian hedgehog (Ihh) displayed the highest downregulation among the ovary enriched genes. IHH regulated genes including Hhip as well as the steroidogenic enzymes were also downregulated in Esr2KO rat ovaries. Remarkably, the expression of Ihh in Esr2KO ovaries was not upregulated despite the high levels of Gdf9 and Bmp15, which are known regulators of Ihh expression in granulosa cells. Our findings suggest that indian hedgehog signaling in the neonatal rat ovary is dependent on ESR2.

scholarly journals Differential distribution of gelatinases and tissue inhibitor of metalloproteinase-1 in the rat ovary

1998 ◽  
Vol 158 (2) ◽  
pp. 221-228 ◽  
Author(s):  
P Bagavandoss
Keyword(s):  
Plasma Membrane ◽  
Corpus Luteum ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Neonatal Rat ◽  
Luteal Cell ◽  
Surface Epithelium ◽  
Tissue Inhibitor ◽  
Differential Distribution ◽  
Thecal Cells ◽  
Rat Ovary

The distribution of gelatinases/matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in neonatal and gonadotropin-primed immature rat ovaries was studied by immunofluorescent microscopy. Immature female Long-Evans rats were primed with 15 IU pregnant mare's serum gonadotropin (PMSG) in 100 microliters PBS. Two days later, to induce ovulation, the rats were injected with human chorionic gonadotropin (hCG, 5 IU/100 microliters PBS). The animals were killed at appropriate times and the ovaries removed and processed for cryostat or paraffin sectioning. Ovaries were also obtained from 7-day-old neonatal rats and processed as above. In the neonatal rat ovary, MMP-2 was present in the follicle and in the ovarian surface epithelium. MMP-9 was not detectable in the neonatal ovary. TIMP-1 was present in the oocyte and in the surface epithelium. In the PMSG-primed ovary, MMP-2 was present in the granulosa and thecal cells of the ovary. MMP-9 distribution, however, was restricted to the interstitial and thecal cells. TIMP-1 was mainly present in the blood vessels and thecal cells, with minor staining in the granulosa cells. In the developing corpus luteum, luteal and endothelial cells were positive for MMP-2. MMP-9 localization was restricted to the plasma membrane of the luteal and interstitial cells. TIMP-1 was clearly observed in the luteal capillaries and, to a lesser extent, in the luteal cell plasma membrane. This distribution of MMP-2, MMP-9, and TIMP-1 in the corpus luteum persisted throughout the life span of the corpus luteum. The spatial and temporal distribution of the gelatinases and TIMP-1 suggests unique roles for these proteins in the rat ovary.

The effects of bisphenol A in in vitro neonatal rat ovary

2014 ◽  
Author(s):  
Korhan Altunbas ◽  
Artay Yagci ◽  
Sefa Celik ◽  
Ozlem Ozden Akkaya ◽  
Berrin Zik
Keyword(s):  
Bisphenol A ◽  
Neonatal Rat ◽  
Rat Ovary

Ontogeny of gonadotrophin receptors and gonadotrophin-stimulated cyclic AMP production in the neonatal rat ovary

1990 ◽  
Vol 127 (2) ◽  
pp. 297-303 ◽  
Author(s):  
T. Sokka ◽  
I. Huhtaniemi
Keyword(s):  
Cyclic Amp ◽  
Cholera Toxin ◽  
Specific Binding ◽  
The Body ◽  
Neonatal Rat ◽  
Female Rats ◽  
Fetal Life ◽  
Camp Production ◽  
Rat Ovary

ABSTRACT The sequence of appearance of FSH and LH receptors, and response of cyclic AMP (cAMP) production to these hormones and cholera toxin, were studied in the fetal and neonatal rat ovary. Specific binding of radio-labelled human (h)FSH and chorionic gonadotrophin (CG) to ovarian homogenates was first detectable on day 7 of life. The content of FSH receptors per ovary increased tenfold between days 7 and 16, and that of LH receptors 27-fold. A significant response of cAMP production in vitro to FSH appeared on day 4 of life, but no significant effect of hCG on cAMP was achieved until day 7. In contrast, cholera toxin had a marked effect on cAMP production by day 17 of fetal life. Although both FSH and LH receptors were detectable in the neonatal rat ovary by day 7, the present findings indicate that the FSH responsiveness of the ovary appears earlier than that of LH. The post-receptor machinery of cAMP production is already functional in the fetal ovary as shown by the experiments with cholera toxin. The appearance of the receptor may therefore be the last link in the ontogeny of the gonadotrophin signal transduction system in the ovary. To study the hormone dependence of the appearance of gonadotrophin responsiveness, neonatal female rats were treated on days 1–6 or 1–9 of life with a potent gonadotrophin-releasing hormone antagonist, and killed on the following day. In both treatment groups, the pituitary LH and FSH contents were suppressed. The body weights remained unaltered, but ovarian weights decreased significantly during both periods of treatment (days 1–6,26·1%, P < 0·05; days 1–9,54·0%, P <0·001). No difference in basal or FSH-stimulated cAMP production was achieved by antagonist treatment for the first 6 days of life. The basal and hCG-stimulated rates of cAMP production per ovary were reduced in animals treated for 9 days (P <0·01), but the FSH-stimulated cAMP production remained unaffected. Hence, whereas the responsiveness to FSH seems to develop in the absence of normal gonadotrophin secretion, a causal relationship between normal gonadotrophin levels and the appearance of LH/hCG responsiveness is apparent in the neonatal rat ovary. Journal of Endocrinology (1990) 127, 297–303

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