Neuropeptide Y directly reduced apoptosis of granulosa cells, and the expression of NPY and its receptors in PCOS subjects

Background Most women with anovulatory infertility show polycystic ovarian syndrome (PCOS), and androgen excess is known as a key factor involved in pathogenicity of PCOS. However, the mechanism of follicular developmental arrest in PCOS is not completely understood. The reproductive function of Neu...

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Published in:Journal of ovarian research Vol. 16; no. 1; pp. 1 - 10
Main Authors: Urata, Yoko, Salehi, Reza, Wyse, Brandon A., Jahangiri, Sahar, Librach, Clifford L., Tzeng, Chii-Ruey, Osuga, Yutaka, Tsang, Benjamin
Format: Journal Article
Language:English
Published: London BioMed Central 31.08.2023
BioMed Central Ltd
Springer Nature B.V
BMC
Subjects:
Analysis
Androgens
Apoptosis
Body fat
Cell culture
Cell growth
Cell proliferation
Dihydrotestosterone
Enzyme-linked immunosorbent assay
Follicular fluid
Folliculogenesis
Granulosa cells
Gynecology
Hyperandrogenism
Infertility
Medicine
Medicine & Public Health
Metabolism
mRNA
Neuropeptide
Neuropeptide Y
Neuropeptides
Ovaries
Pathogenesis
Pathogenicity
Phenotypes
Polycystic ovarian syndrome
Polycystic ovary syndrome
Protein folding
Proteins
Receptor mechanisms
Reproductive Medicine
RNA
Stein-Leventhal syndrome
Neuropeptide Y
Polycystic ovarian syndrome
Hyperandrogenism
Neuropeptide
Apoptosis
ISSN:1757-2215, 1757-2215
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Summary:Background Most women with anovulatory infertility show polycystic ovarian syndrome (PCOS), and androgen excess is known as a key factor involved in pathogenicity of PCOS. However, the mechanism of follicular developmental arrest in PCOS is not completely understood. The reproductive function of Neuropeptide Y (NPY) in the ovary during folliculogenesis was previously reported; NPY function in apoptosis and proliferation of granulosa cells (GCs) is follicular-stage dependent. The objective of this study was to investigate the role of NPY in ovarian follicular development and the pathogenesis of PCOS. Methods To simulate the PCOS phenotype using a rat model, 21-day old Sprague Dawley rats were implanted with dihydrotestosterone (DHT) capsule (83 µg/day) and euthanized after 28 days. mRNA and protein content of NPY and its receptors were assessed in GCs from DHT treated rats using RT-qPCR and Western blot, respectively. Proliferation and apoptosis of GCs was assessed using Ki67- and TUNEL assays. Finally, NPY levels were measured in human follicular fluid (FF) from matched PCOS and non-PCOS patients using ELISA. Results GCs from DHT treated rats (PCOS-GCs) contained significantly less NPY protein and Npy mRNA by 0.16- and 0.56-fold, respectively, and more NPY receptor type 2 and 5 protein by 2.21- and 3.17-fold, respectively, when compared to sham control. Addition of recombinant NPY to PCOS-GCs culture did not alter Ki67-positive but significantly decreased TUNEL-positive cells by 0.65-fold, but not to baseline levels. There was no significant difference in NPY levels in FF between PCOS and non-PCOS subjects. Conclusions These results indicate that DHT modulates expression of NPY and its receptors, NPY decreases DHT-induced GCs apoptosis. That alterations in NPY’s function might be involved in follicular developmental failure of PCOS.
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ISSN:1757-2215
1757-2215
DOI:10.1186/s13048-023-01261-8