Roles of different n-3/n-6 PUFA ratios in ovarian cell development and steroidogenesis in PCOS rats

2019 ◽  
Vol 10 (11) ◽  
pp. 7397-7406 ◽  
Author(s):  
Xiaoshu Ma ◽  
Xuechun Weng ◽  
Xusong Hu ◽  
Qiaozhi Wang ◽  
Ye Tian ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Growth Arrest ◽  
Cell Development ◽  
Follicle Growth ◽  
Ovary Syndrome ◽  
Ovarian Cell ◽  
Endocrine Disorder

Polycystic ovary syndrome (PCOS) is a complex and common endocrine disorder characterized by hyperandrogenism, which is accompanied by follicle growth arrest at the small antral stage, minimal granulosa cell proliferation, and chronic anovulation.

scholarly journals miR-3188 Regulates proliferation and apoptosis of granulosa cells by targeting KCNA5 in the polycystic ovary syndrome

2021 ◽  
Author(s):  
Shan Zhou ◽  
Liang Xia ◽  
Yuanyuan Chen ◽  
Weiying Guo ◽  
Jinxing Hu
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Polycystic Ovary Syndrome ◽  
Cell Viability ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Polycystic Ovary ◽  
Healthy Controls ◽  
Ovarian Dysfunction ◽  
Ovary Syndrome

Abnormal proliferation of granulosa cells is implicated in ovarian dysfunction and dysregulated folliculogenesis in the polycystic ovary syndrome (PCOS). Aberrant microRNA (miRNA) expression might contribute to disordered folliculogenesis and granulosa cell proliferation in PCOS. This study aimed to investigate the roles of miR-3188 in ovarian dysfunction, as well as the mechanism involved in granulosa cell proliferation in PCOS. Firstly, peripheral blood samples were isolated from PCOS patients and healthy controls, and qRT-PCR analysis demonstrated a dramatic increase in miR-3188 in PCOS patients when compared to the healthy controls. Secondly, miR-3188 overexpression increased cell viability of the granulosa-like tumor cell line (KGN). However, cell viability of KGN was repressed by interference with miR-3188. MiR-3188 promoted cell cycle of KGN through increasing cyclinD1 and decreasing p21 levels. Moreover, cell apoptosis was suppressed by miR-3188 in KGN, indicated by enhanced Bcl-2, and reduced Bax and cleaved caspase-3 levels, whereas knockdown of miR-3188 resulted in opposite effects. Lastly, potassium voltage-gated channel subfamily A member 5 (KCNA5) was verified as a target of miR-3188. KCNA5 expression was decreased and displayed negative correlation with miR-3188 levels in PCOS patients. Overexpression of KCNA5 attenuated the promotive effects of miR-3188 on cell viability and cell cycle in KGN. In conclusion, miR-3188, a key miRNA enhanced in PCOS, promoted granulosa cell proliferation through down-regulation of KCNA5, providing a new therapeutic target for PCOS.

MiR-let-7d-3p inhibits granulosa cell proliferation by targeting TLR4 in polycystic ovary syndrome

2021 ◽  
Author(s):  
Wei Wu ◽  
Cuicui Duan ◽  
Houyi Lv ◽  
Jianyuan Song ◽  
Wangyu Cai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Polycystic Ovary Syndrome ◽  
Granulosa Cell ◽  
Polycystic Ovary ◽  
Ovary Syndrome

scholarly journals Polycystic Ovary Syndrome: Familiar to Millions?

2020 ◽  
Vol 10 (1) ◽  
pp. 1
Author(s):  
Johannes Ott
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Psychological Consequences ◽  
Ovary Syndrome ◽  
Endocrine Disorder ◽  
High Prevalence ◽  
Basic Characteristics

Often, articles about polycystic ovary syndrome (PCOS) start with information about the condition’s high prevalence, the basic characteristics that define this endocrine disorder, and the manifold somatic and/or psychological consequences [...]

Impacts of Metformin on Local Ovarian Cell Tissue of Rats with Polycystic Ovary Syndrome and Intestinal Flora Under Aerobic Exercise

2021 ◽  
Vol 11 (12) ◽  
pp. 2381-2388
Author(s):  
Xiao Yan
Keyword(s):  
Growth Factor ◽  
Polycystic Ovary Syndrome ◽  
Aerobic Exercise ◽  
Polycystic Ovary ◽  
Ovarian Tissue ◽  
Ovary Syndrome ◽  
Ovarian Cell ◽  
Expression Levels ◽  
Cell Tissue ◽  
Igf I

In order to explore the possible treatment mechanism of metformin on the local ovarian cell tissue of rats with polycystic ovary syndrome (PCOS), 35 female clean sterile rats were selected as the research objects in this study, and randomly divided a PCOS model group (PCOS MG) (25 rats) and a control group (CG) (10 rats). After the modelling was completed, 5 rats were randomly selected to evaluate the modelling effect. When the success rate was higher than 80%, the remaining model rats were divided into two groups randomly, namely the (PCOS MG) (10 rats) and the treatment group (TG) (10 rats). Hematoxylin-eosin (HE) staining was performed on ovarian tissue of the rat, and the ovarian tissue structure was observed under light microscope. Immunohistochemistry was used to detect the distribution and expression levels of tumour necrosis factor-α (TNF-α), insulin-like growth factor-I (IGF-I), and connective tissue growth factor (CTGF) on the ovaries of rats in each group. It was found by observing the vaginal smear under the microscope that the rats in the (PCOS MG) had lost the regular estrous cycle, suggesting that there was no ovulation. The expression levels of TNF-α and CTGF in rats in the (PCOS MG) were greatly higher than those in the CG (P < 0.05); compared with the (PCOS MG), the expression levels of TNF-α and CTGF in the TG were decreased observably (P < 0.05). IGF-I was mainly expressed in granulosa cells (GCs) and follicular membrane cells (FMCs) of the ovarian tissue. The expression level of IGF-I in ovarian GCs in rats in the (PCOS MG) was significantly higher than that in the CG (P < 0.05). The expression level of IGF-I in GCs in the TG was lower significantly than that in the (PCOS MG) (P < 0.05). By comparing with rats in the CG, the rats in the (PCOS MG) had obviously decreased Actinobacteria and Betaproteobacteria in the intestinal tract, and the proportion of Firmicutes in the intestine was significantly increased; the amount of butyric acid in the faeces of rats with aerobic exercise was obviously higher than that in the (PCOS MG), because exercise increased the proportion of intestinal butyric acid-producing bacteria. Conclusion: metformin combined with aerobic exercise can treat the PCOS by regulating serum hormone levels and the expression levels of TNF-α, IGF-I, and CTGF.

scholarly journals LncRNA TMPO-AS1 suppresses the maturation of miR-335-5p to participate in polycystic ovary syndrome

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Fang Hou ◽  
Jie Li ◽  
Jie Peng ◽  
Zhenghua Teng ◽  
Jun Feng ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Polycystic Ovary Syndrome ◽  
Follicular Fluid ◽  
Polycystic Ovary ◽  
Subcellular Location ◽  
Ovary Syndrome ◽  
Brdu Assay ◽  
Transfection Assay

Abstract Background TMPO-AS1 is a recently characterized oncogenic lncRNA in ovarian cancer. Its role in other ovary diseases is unknown. This study explored its role in polycystic ovary syndrome (PCOS). Methods Follicular fluid was extracted from both PCOS patients and controls. The levels of TMPO-AS1 and mature and premature miR-335-5p were analyzed by RT-qPCR. The role of TMPO-AS1 in regulating miR-355-5p maturation in granulosa-like tumor (KGN) cells was analyzed by overexpression experiments. The interaction between TMPO-AS1 and premature miR-335-5p was analyzed by RNA pull-down assay. The subcellular location of TMPO-AS1 in KGN cells was analyzed by nuclear fractionation assay. The role of TMPO-AS1 and miR-335-5p in KGN cell proliferation was analyzed by BrdU assay. Results TMPO-AS1 was increased in PCOS, while mature miR-355-5p was decreased in PCOS. TMPO-AS1 overexpression decreased mature miR-355-5p level but increased premature miR-355-5p. TMPO-AS1 was localized in both nucleus and cytoplasm. TMPO-AS1 directly interacted with premature miR-355-5p in KGN cells. TMPO-AS1 increased KGN cell proliferation while miR-355-5p decreased cell proliferation. The co-transfection assay showed that TMPO-AS1 reduced the suppressive effects of miR-355-5p on cell proliferation. Conclusions TMPO-AS1 might suppress miR-335-5p maturation to participate in PCOS.

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