MicroRNA-9119 regulates cell viability of granulosa cells in polycystic ovarian syndrome via mediating Dicer expression

2020 ◽  
Vol 465 (1-2) ◽  
pp. 187-197
Author(s):  
Yang Ding ◽  
Pei He ◽  
Zhiling Li
Keyword(s):  
Cell Viability ◽  
Granulosa Cells ◽  
Polycystic Ovarian Syndrome ◽  
Dicer Expression ◽  
Ovarian Syndrome

scholarly journals miR‑132 is upregulated in polycystic ovarian syndrome and inhibits granulosa cells viability by targeting Foxa1

2020 ◽  
Vol 22 (6) ◽  
pp. 5155-5162
Author(s):  
Xiangrong Cui ◽  
Xuan Jing ◽  
Junfen Liu ◽  
Xingyu Bi ◽  
Xueqing Wu
Keyword(s):  
Granulosa Cells ◽  
Polycystic Ovarian Syndrome ◽  
Ovarian Syndrome

Fractalkine and apoptotic/anti-apoptotic markers in granulosa cells of women with polycystic ovarian syndrome

2020 ◽  
Vol 47 (5) ◽  
pp. 3593-3603
Author(s):  
Aydin Raei Sadigh ◽  
Masoud Darabi ◽  
Ali Salmassi ◽  
Kobra Hamdi ◽  
Laya Farzadi ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Polycystic Ovarian Syndrome ◽  
Apoptotic Markers ◽  
Ovarian Syndrome

Expression of inhibin α,βA and βB messenger ribonucleic acids in the normal human ovary and in polycystic ovarian syndrome

1994 ◽  
Vol 143 (1) ◽  
pp. 127-137 ◽  
Author(s):  
T-A Jaatinen ◽  
T-L Penttilä ◽  
A Kaipia ◽  
T Ekfors ◽  
M Parvinen ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Cellular Localization ◽  
Polycystic Ovarian Syndrome ◽  
Human Ovary ◽  
Α Subunit ◽  
Ribonucleic Acids ◽  
Theca Cells ◽  
Subunit Mrna ◽  
Normal Human ◽  
Ovarian Syndrome

Abstract We studied the cellular distribution of inhibin α, βA and βB mRNAs in the normal human ovary and in polycystic ovarian syndrome (PCOS) by in situ hybridization. Our results show that human granulosa cells express inhibin α, βA and βB subunit mRNAs, and theca cells express inhibin α and βA subunit mRNAs. The co-localization of α and βA mRNAs in theca cells supports the hypothesis that inhibin also has an autocrine function in these cells. We did not detect any inhibin subunit mRNA in the granulosa cells of atretic follicles, while theca cells also expressed α subunit mRNA in those follicles. The present findings suggest that the expression of inhibin subunits is regulated differently in human follicular granulosa and theca cells. It has been speculated that inhibin may be involved in the development of PCOS. Our results show that the cellular localization of inhibin subunit mRNAs is not disturbed in PCOS ovaries. Journal of Endocrinology (1994) 143, 127–137

scholarly journals Insulin and Insulin-Like Growth Factor Stimulation of Vascular Endothelial Growth Factor Production by Luteinized Granulosa Cells: Comparison between Polycystic Ovarian Syndrome (PCOS) and Non-PCOS Women

2007 ◽  
Vol 92 (7) ◽  
pp. 2726-2733 ◽  
Author(s):  
Meghan B. Stanek ◽  
Sherri M. Borman ◽  
Theodore A. Molskness ◽  
Janine M. Larson ◽  
Richard L. Stouffer ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Granulosa Cells ◽  
Polycystic Ovarian Syndrome ◽  
Culture Media ◽  
Vascular Endothelial ◽  
Vitro Fertilization ◽  
Endothelial Growth Factor ◽  
Ovarian Syndrome

Abstract Context: Vascular endothelial growth factor A (VEGF-A) is a potent cytokine that promotes angiogenesis and vascular permeability. After controlled ovarian stimulation (COS) for in vitro fertilization (IVF), excessive VEGF-A production can occur, particularly in women with polycystic ovarian syndrome (PCOS); however, it is unclear whether the regulation of VEGF-A production is different between PCOS and non-PCOS women. Objective: The aim of this study was to determine whether there were differences in the dose- and time-dependent effects of insulin and IGFs on VEGF-A production by luteinized granulosa cells (LGCs) from women with and without PCOS. Design and Setting: A prospective comparative experimental study was conducted at an institutional practice. Patients: Patients included six PCOS and six non-PCOS women undergoing COS and IVF. Interventions: Interventions included COS for IVF. Main Outcome Measures: VEGF-A levels in culture media were collected daily for 3 d from LGCs after incubation with variable doses of insulin, IGF-I, and IGF-II in the presence and absence of LH. Results: In both study groups, exposure to LH alone did not alter VEGF-A levels. However, insulin or IGF increased VEGF-A levels within 1 d and appeared to synergize with LH at 3 d. VEGF-A production by non-PCOS LGCs was more sensitive to IGF exposure, whereas PCOS cells were more sensitive to insulin. Although an increase in DNA content (P < 0.05) was noted in cultures of PCOS cells, progesterone levels were lower compared with non-PCOS LGCs. Conclusion: Insulin and IGFs promote VEGF-A production in LGCs, but the response patterns are different when cells from PCOS and non-PCOS women are compared.

scholarly journals Non-canonical progesterone signaling in granulosa cell function

Reproduction ◽  
2014 ◽  
Vol 147 (5) ◽  
pp. R169-R178 ◽  
Author(s):  
John J Peluso ◽  
James K Pru
Keyword(s):  
Granulosa Cell ◽  
Granulosa Cells ◽  
Polycystic Ovarian Syndrome ◽  
Cell Function ◽  
Reproductive Capacity ◽  
Dependent Manner ◽  
Follicle Growth ◽  
Altered Expression ◽  
Ovarian Syndrome ◽  
Enhancer Factor

It has been known for over 3 decades that progesterone (P4) suppresses follicle growth. It has been assumed that P4 acts directly on granulosa cells of developing follicles to slow their development, as P4 inhibits both mitosis and apoptosis of cultured granulosa cells. However, granulosa cells of developing follicles of mice, rats, monkeys, and humans do not express the A or B isoform of the classic nuclear receptor for P4 (PGR). By contrast, these granulosa cells express other P4 binding proteins, one of which is referred to as PGR membrane component 1 (PGRMC1). PGRMC1 specifically binds P4 with high affinity and mediates P4's anti-mitotic and anti-apoptotic action as evidenced by the lack of these P4-dependent effects in PGRMC1-depleted cells. In addition, mice in which PGRMC1 is conditionally depleted in granulosa cells show diminished follicle development. While the mechanism through which P4 activation of PGRMC1 affects granulosa cell function is not well defined, it appears that PGRMC1 controls granulosa cell function in part by regulating gene expression in T-cell-specific transcription factor/lymphoid enhancer factor-dependent manner. Clinically, altered PGRMC1 expression has been correlated with premature ovarian failure/insufficiency, polycystic ovarian syndrome, and infertility. These collective studies provide strong evidence that PGRMC1 functions as a receptor for P4 in granulosa cells and that altered expression results in compromised reproductive capacity. Ongoing studies seek to define the components of the signal transduction cascade through which P4 activation of PGRMC1 results in the regulation of granulosa cell function.

scholarly journals Chemerin, a Novel Regulator of Follicular Steroidogenesis and Its Potential Involvement in Polycystic Ovarian Syndrome

Endocrinology ◽  
2012 ◽  
Vol 153 (11) ◽  
pp. 5600-5611 ◽  
Author(s):  
Qi Wang ◽  
Ji Young Kim ◽  
Kai Xue ◽  
Jia-yin Liu ◽  
Arthur Leader ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Polycystic Ovarian Syndrome ◽  
Regulatory Protein ◽  
Hydroxysteroid Dehydrogenase ◽  
Negative Regulator ◽  
Estradiol Secretion ◽  
Chain Cleavage ◽  
Steroidogenic Acute Regulatory ◽  
Ovarian Syndrome

Abstract Polycystic ovarian syndrome (PCOS) is a heterogeneous syndrome associated with follicle growth arrest, minimal granulosa cell proliferation, dysregulated sex hormone profile, hyperthecosis, and insulin resistance. Using a 5α-dihydrotestosterone (DHT)-induced rat model that recapitulates the reproductive and metabolic phenotypes of human PCOS, we have examined the steroidogenic capability of granulosa cells from DHT-treated rats. Gene expression of several key steroidogenic enzymes including p450 side-chain cleavage enzyme (p450scc), aromatase, steroidogenic acute regulatory protein, hydroxysteroid dehydrogenase-17β, and hydroxysteroid dehydrogenase-3β were markedly lower in DHT-treated rats than the controls, although the responsiveness of their granulosa cells to FSH was higher. Expression of the adipokine chemerin and its receptor, chemokine receptor-like 1, was evident in control and DHT-treated rats, with significantly higher ovarian mRNA abundances and protein contents of chemerin and its receptor. Recombinant chemerin decreases basal estradiol secretion in granulosa cells from DHT-treated rats. When the inhibitory role of chemerin on steroidogenesis was further examined in vitro, chemerin suppressed FSH-induced progesterone and estradiol secretion in cultured preantral follicles and granulosa cells. Chemerin also inhibits FSH-induced aromatase and p450scc expression in granulosa cells. Overexpression of nuclear receptors NR5a1 and NR5a2 promotes p450scc and aromatase expression, respectively, which is suppressed by chemerin. These findings suggest that chemerin is a novel negative regulator of FSH-induced follicular steroidogenesis and may contribute to the pathogenesis of PCOS.

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