scholarly journals Induction of Ski Protein Expression upon Luteinization in Rat Granulosa Cells

2012 ◽  
Vol 25 (5) ◽  
pp. 635-641 ◽  
Author(s):  
Hyun Kim ◽  
Dong Hun Kim ◽  
Soo Bong Park ◽  
Yeoung-Gyu Ko ◽  
Sung-woo Kim ◽  
...  
2012 ◽  
Vol 58 (2) ◽  
pp. 254-259
Author(s):  
Hyun KIM ◽  
Keitaro YAMANOUCHI ◽  
Takashi MATSUWAKI ◽  
Masugi NISHIHARA

Zygote ◽  
2016 ◽  
pp. 1
Author(s):  
Hyun Kim ◽  
Young Moo Cho ◽  
Yeoung-Gyu Ko ◽  
Changyong Choe ◽  
Hwan-Hoo Seong

Zygotewishes to inform its readers that its Editor-in-Chief has decided to retract the above article after an investigation carried out in compliance with the Committee on Publication Ethics guidelines found that the authors duplicated substantial parts of the following two articles:1.Kim H, Yamanouchi K, Nishihara M. (2006) Expression of ski in the granulosa cells of atretic follicles in the rat ovary.J. Reprod. Dev.52, 715–7212.Kim H, Yamanouchi K, Matsuwaki T, Nishihara M. (2012) Induction of Ski protein expression upon luteinization in rat granulosa cells without a change in its mRNA expression.J. Reprod. Dev.58, 254–259


2013 ◽  
Vol 61 (1) ◽  
pp. 85-98 ◽  
Author(s):  
Anna Nynca ◽  
Dominika Słonina ◽  
Olga Jablońska ◽  
Barbara Kamińska ◽  
Renata Ciereszko

Daidzein, a phytoestrogen present in soybean products used in swine feed, has been demonstrated to affect both reproductive and endocrine functions. The aims of this study were to examine the in vitro effects of daidzein on (1) progesterone (P4) and oestradiol (E2) secretion by porcine luteinised granulosa cells harvested from medium follicles, and (2) the mRNA and protein expression of oestrogen receptors α and β (ERα and ERβ) in these cells. The influence of E2 on P4 secretion and ERα and ERβ expression in the granulosa cells of pigs was also investigated. It was found that daidzein inhibited progesterone secretion by luteinised granulosa cells isolated from medium follicles. In contrast, E2 did not affect progesterone production by these cells. Moreover, daidzein did not alter the granulosal secretion of E2. Both daidzein and E2 decreased mRNA expression of ERα in the cells examined. The expression of ERβ mRNA was not affected by daidzein but was inhibited by E2. ERα protein was not detected while ERβ protein was found in the nuclei of the cells. Daidzein and E2 upregulated the expression of ERβ protein in the cells. In summary, the phytoestrogen daidzein directly affected the porcine ovary by inhibiting progesterone production and increasing ERβ protein expression. Daidzein-induced changes in follicular steroidogenesis and granulosal sensitivity to oestrogens may disturb reproductive processes in pigs.


2020 ◽  
Vol 103 (3) ◽  
pp. 608-619
Author(s):  
Ping Zhong ◽  
Jin Liu ◽  
Hong Li ◽  
Senbin Lin ◽  
Lingfeng Zeng ◽  
...  

Abstract This study aimed to investigate whether cadmium (Cd) cytotoxicity in rat ovarian granulosa cells (OGCs) is mediated through apoptosis or autophagy and to determine the role of microRNAs (miRNAs) in Cd cytotoxicity. To test this hypothesis, rat OGCs were exposed to 0, 10, and 20 μM CdCl2 in vitro. As the Cd concentration increased, OGC apoptosis increased. In addition, Cd promoted apoptosis by decreasing the mRNA and protein expression levels of inhibition of B-cell lymphoma 2 (Bcl2). However, under our experimental conditions, no autophagic changes in rat OGCs were observed, and the mRNA and protein expression levels of the autophagic markers microtubule-associated protein 1 light chain 3 alpha (Map1lc3b) and Beclin1 (Becn1) were not changed. Microarray chip analysis, miRNA screening, and bioinformatics approaches were used to further explore the roles of apoptosis regulation-related miRNAs. In total, 19 miRNAs putatively related to Cd-induced apoptosis in rat OGCs were identified. Notably, miR-204-5p, which may target Bcl2, was identified. Then, rat OGCs were cultured in vitro and used to construct the miR-204-5p-knockdown cell line LV2-short hairpin RNA (shRNA). LV2-shRNA cells were exposed to 20 μM Cd for 12 h, and the mRNA and protein expression levels of Bcl2 were increased. Our findings suggest that Cd is cytotoxic to rat OGCs, and mitochondrial apoptosis rather than autophagy mediates Cd-induced damage to OGCs. Cd also affects apoptosis-related miRNAs, and the underlying apoptotic mechanism may involve the Bcl2 gene.


2020 ◽  
Vol 33 (4) ◽  
pp. 547-555 ◽  
Author(s):  
Xiaodong Zhang ◽  
Qiangqiang Tao ◽  
Jinnan Shang ◽  
Yiliang Xu ◽  
Liang Zhang ◽  
...  

Objective: Apoptosis of ovarian granulosa cells (GCs) affects mammalian follicular development and fecundity. This study aimed to explore the regulatory relationship between microRNA-26a (miR-26a) and the 3β-hydroxysteroid-Δ24-reductase gene (<i>DHCR24</i>) gene in porcine follicular granular cells (pGCs), and to provide empirical data for the development of methods to improve the reproductive capacity of pigs.Methods: The pGCs were transfected with miR-26a mimic, miR-26a inhibitor and <i>DHCR24</i>-siRNA <i>in vitro</i>. The cell apoptosis rate of pGCs was detected by the flow cytometry. The secretion levels of estradiol (E2) and progesterone (P) in pGCs were detected by enzymelinked immunosorbent assay. Double luciferase validation system was used to detect the binding sites between miR-26a and <i>DHCR24</i> 3′-UTR region. Qualitative real-time polymerase chain reaction and Western blotting were used to verify the <i>DHCR24</i> mRNA and protein expression in pGCs, respectively, after transfecting with miR-26a mimic and miR-26a inhibitor.Results: Results showed that enhancement of miR-26a promoted apoptosis, and inhibited E2 and P secretion in pGCs. Meanwhile, inhibition of <i>DHCR24</i> also upregulated the Caspase-3 expression, reduced the BCL-2 expression, promoted pGCs apoptosis, and inhibited E2 and P secretion in pGCs. There were the binding sites of miR-26a located within <i>DHCR24</i> 3′-UTR. Up-regulation of miR-26a inhibited <i>DHCR24</i> mRNA and protein expression in pGCs.Conclusion: This study demonstrates that miR-26a can promote cell apoptosis and inhibit E2 and P secretion by inhibiting the expression of <i>DHCR24</i> in pGCs.


Reproduction ◽  
1995 ◽  
Vol 104 (1) ◽  
pp. 77-83 ◽  
Author(s):  
A. L. Bernal ◽  
J. Bellinger ◽  
J. M. Marshall ◽  
S. Phaneuf ◽  
G. N. Europe-Finner ◽  
...  

Reproduction ◽  
2009 ◽  
Vol 137 (5) ◽  
pp. 865-877 ◽  
Author(s):  
Hugo H Ortega ◽  
Natalia R Salvetti ◽  
Vasantha Padmanabhan

Steroid hormones play an important role in reproduction and the receptors through which they signal change in a developmental time, follicle stage, and cell-specific manner. Disruption in steroid receptor expression affects follicle formation and differentiation. In this study, using prenatal testosterone (T) and dihydrotestosterone (DHT)-treated female sheep as model systems, we tested the hypothesis that prenatal androgen excess disrupts the developmental ontogeny of ovarian steroid receptor protein expression. Pregnant Suffolk ewes were injected twice weekly with T propionate or DHT propionate (a non-aromatizable androgen) in cottonseed oil from days 30 to 90 of gestation. Changes in ovarian estrogen receptors (ER; ESR1, ESR2), androgen receptor (AR) and progesterone receptor (PGR) proteins were determined at fetal (days 90 and 140), postpubertal (10 months), and adult (21 months; only prenatal T-treated sheep studied) ages by immunohistochemistry. Prenatal T and DHT treatment induced selective increase in AR but not ER or PGR expression in the stroma and granulosa cells of fetal days 90 and 140 ovaries. An increase in ESR1 and decrease in ESR2 immunostaining coupled with increased AR expression were evident in granulosa cells of antral follicles of 10- and 21-month-old prenatal T but not DHT-treated females (analyzed only at 10 months). These findings provide evidence that an early increase in ovarian AR is the first step in the altered ovarian developmental trajectory of prenatal T-treated females, and manifestations of postnatal ovarian dysfunction are likely facilitated via altered equilibrium of antral follicular granulosa cell ER/AR protein expression.


2019 ◽  
Vol 234 (11) ◽  
pp. 20240-20248
Author(s):  
Ali Salmassi ◽  
Amir Fattahi ◽  
Nora Simon ◽  
Zeinab Latifi ◽  
Tohid Ghasemnejad ◽  
...  

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