scholarly journals Paeoniflorin attenuates DHEA-induced polycystic ovary syndrome via inactivation of TGF-β1/Smads signaling pathway in vivo

Aging ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 7084-7095
Author(s):  
Jie Zhou ◽  
Yong Tan ◽  
Xudong Wang ◽  
Meihong Zhu
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Tgf Β1

Notch signaling pathway in cumulus cells reflecting zygote and embryo quality in polycystic ovary syndrome

2021 ◽  
Author(s):  
Mojtaba Masoudi ◽  
Nazila Yamini ◽  
Fahimeh Salehi ◽  
Reza Aflatoonian ◽  
Maryam Azizi Kutenaee ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Embryo Quality ◽  
Polycystic Ovary ◽  
Cumulus Cells ◽  
Notch Signaling Pathway ◽  
Ovary Syndrome

scholarly journals Adiponectin Reduces Embryonic Loss Rate and Ameliorates Trophoblast Apoptosis in Early Pregnancy of Mice with Polycystic Ovary Syndrome by Affecting the AMPK/PI3K/Akt/FoxO3a Signaling Pathway

2020 ◽  
Vol 27 (12) ◽  
pp. 2232-2241 ◽  
Author(s):  
Wenqian Zhang ◽  
Meng Zuo ◽  
Juan Lu ◽  
Yuxia Wang
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Early Pregnancy ◽  
Loss Rate ◽  
Polycystic Ovary ◽  
Uterine Tissue ◽  
Trophoblast Cells ◽  
Ovary Syndrome ◽  
Villous Trophoblast ◽  
Embryo Loss

Abstract Reports in recent years have suggested that adiponectin (APN) improves insulin resistance and inhibits apoptosis by activating the AMP-activated protein kinase (AMPK) pathway and the PI3K/Akt signaling pathway after binding to its receptor. This study aims to explore the mechanism by which APN reduces embryo loss rate and trophoblast apoptosis in early pregnancy of mice with polycystic ovary syndrome (PCOS). PCOS mice were subcutaneously injected with APN (10 μg mg kg−1 day−1) on 11 consecutive days from the 3rd day of pregnancy onwards to observe the change of the embryo loss rate of PCOS mice induced by APN. Quantitative real-time PCR and Western blot were used to determine the relative expressions of mRNA and the proteins AMPK, PI3K, and Akt in mouse uterine tissue. At the same time, primary cultured mouse villous trophoblast cells were used to further explore the underlying mechanisms in vitro. APN significantly reduces the pregnancy loss rate of PCOS mice. At the same time, APN increases phosphorylation and mRNA expression levels of AMPK, PI3K, and Akt in PCOS mouse uterine tissue. In addition, trophoblast cells of model mice were treated with APN and inhibitors, and APN was found to reduce trophoblast cell apoptosis by affecting the phosphorylation levels of AMPK, PI3K, Akt, and FoxO3a proteins. APN reduces the embryo loss rate and ameliorates trophoblast apoptosis in PCOS mice by affecting the AMPK/PI3K/AKT/FoxO3a signaling pathway.

scholarly journals PAPSS2 Deficiency Causes Androgen Excess via Impaired DHEA Sulfation—In Vitro and in Vivo Studies in a Family Harboring Two Novel PAPSS2 Mutations

2015 ◽  
Vol 100 (4) ◽  
pp. E672-E680 ◽  
Author(s):  
Wilma Oostdijk ◽  
Jan Idkowiak ◽  
Jonathan W. Mueller ◽  
Philip J. House ◽  
Angela E. Taylor ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Challenge Test ◽  
Compound Heterozygous ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Functional Impact ◽  
Low Serum

Context: PAPSS2 (PAPS synthase 2) provides the universal sulfate donor PAPS (3′-phospho-adenosine-5′-phosphosulfate) to all human sulfotransferases, including SULT2A1, responsible for sulfation of the crucial androgen precursor dehydroepiandrosterone (DHEA). Impaired DHEA sulfation is thought to increase the conversion of DHEA toward active androgens, a proposition supported by the previous report of a girl with inactivating PAPSS2 mutations who presented with low serum DHEA sulfate and androgen excess, clinically manifesting with premature pubarche and early-onset polycystic ovary syndrome. Patients and Methods: We investigated a family harboring two novel PAPSS2 mutations, including two compound heterozygous brothers presenting with disproportionate short stature, low serum DHEA sulfate, but normal serum androgens. Patients and parents underwent a DHEA challenge test comprising frequent blood sampling and urine collection before and after 100 mg DHEA orally, with subsequent analysis of DHEA sulfation and androgen metabolism by mass spectrometry. The functional impact of the mutations was investigated in silico and in vitro. Results: We identified a novel PAPSS2 frameshift mutation, c.1371del, p.W462Cfs*3, resulting in complete disruption, and a novel missense mutation, c.809G>A, p.G270D, causing partial disruption of DHEA sulfation. Both patients and their mother, who was heterozygous for p.W462Cfs*3, showed increased 5α-reductase activity at baseline and significantly increased production of active androgens after DHEA intake. The mother had a history of oligomenorrhea and chronic anovulation that required clomiphene for ovulation induction. Conclusions: We provide direct in vivo evidence for the significant functional impact of mutant PAPSS2 on DHEA sulfation and androgen activation. Heterozygosity for PAPSS2 mutations can be associated with a phenotype resembling polycystic ovary syndrome.

Polymorphism in postinsulin receptor signaling pathway is not associated with polycystic ovary syndrome

2008 ◽  
Vol 90 (6) ◽  
pp. 2298-2303 ◽  
Author(s):  
Michelle R. Jones ◽  
Scott G. Wilson ◽  
Ben H. Mullin ◽  
Robert Mead ◽  
Frank Dudbridge ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Polycystic Ovary ◽  
Receptor Signaling ◽  
Ovary Syndrome ◽  
Receptor Signaling Pathway
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