scholarly journals MECHANISMS IN ENDOCRINOLOGY: Thyroid and polycystic ovary syndrome

2015 ◽  
Vol 172 (1) ◽  
pp. R9-R21 ◽  
Author(s):  
Simona Gaberšček ◽  
Katja Zaletel ◽  
Verena Schwetz ◽  
Thomas Pieber ◽  
Barbara Obermayer-Pietsch ◽  
...  
Keyword(s):  
Immune Response ◽  
Polycystic Ovary Syndrome ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Reproductive Effects ◽  
Clinical Consequences ◽  
Autoimmune Processes ◽  
Growth Factor Beta

Thyroid disorders, especially Hashimoto's thyroiditis (HT), and polycystic ovary syndrome (PCOS) are closely associated, based on a number of studies showing a significantly higher prevalence of HT in women with PCOS than in controls. However, the mechanisms of this association are not as clear. Certainly, genetic susceptibility contributes an important part to the development of HT and PCOS. However, a common genetic background has not yet been established. Polymorphisms of the PCOS-related gene for fibrillin 3 (FBN3) could be involved in the pathogenesis of HT and PCOS. Fibrillins influence the activity of transforming growth factor beta (TGFβ). Multifunctional TGFβ is also a key regulator of immune tolerance by stimulating regulatory T cells (Tregs), which are known to inhibit excessive immune response. With lower TGFβ and Treg levels, the autoimmune processes, well known in HT and assumed in PCOS, might develop. In fact, lower levels of TGFβ1 were found in HT as well as in PCOS women carrying allele 8 of D19S884 in the FBN3 gene. Additionally, vitamin D deficiency was shown to decrease Tregs. Finally, high estrogen-to-progesterone ratio owing to anovulatory cycles in PCOS women could enhance the immune response. Harmful metabolic and reproductive effects were shown to be more pronounced in women with HT and PCOS when compared with women with HT alone or with controls. In conclusion, HT and PCOS are associated not only with respect to their prevalence, but also with regard to etiology and clinical consequences. However, a possible crosstalk of this association is yet to be elucidated.

Dysregulated miR-142, -33b and -423 in granulosa cells target TGFBR1 and SMAD7: a possible role in polycystic ovary syndrome

2019 ◽  
Vol 25 (10) ◽  
pp. 638-646 ◽  
Author(s):  
Yan Li ◽  
Yungai Xiang ◽  
Yuxia Song ◽  
Lijing Wan ◽  
Guo Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Polycystic Ovary Syndrome ◽  
Granulosa Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Growth Factor Beta ◽  
Tgfb Signaling

Abstract It is well established that microRNA (miRNA) expression profiles are altered in patients with polycystic ovary syndrome (PCOS). In addition, abnormal transforming growth factor beta (TGFB) signaling in granulosa cells is related to the pathological conditions of PCOS. However, the function of dysregulated miRNAs in PCOS is still unclear. In this study, we aimed to elucidate the roles of specific miRNAs in PCOS. We collected follicular fluid from 46 patients with PCOS and 32 healthy controls. Granulosa cells (GCs) were separated and the levels of six candidate miRNAs were determined by quantitative RT-PCR. The direct targets of three dysregulated miRNAs were predicted using bioinformatic tools and confirmed using a dual luciferase assay and immunoblotting. The biological function of three dysregulated miRNAs in primary GCs was determined using a cell proliferation assay and flow cytometry. We found that miR-423 expression was downregulated (P = 0.038), and the levels of miR-33b (P = 0.032) and miR-142 (P = 0.021) were upregulated in GCs from patients with PCOS, compared to controls. miR-423 directly repressed SMAD family member 7 (SMAD7) expression, while transforming growth factor beta receptor 1 (TGFBR1) was a direct target of both miR-33b and miR-142. An RNA oligonucleotide mixture containing miR-423 inhibitor, miR-33b mimic, and miR-142 mimic repressed TGFB signaling, promoted cell proliferation (P = 0.0098), repressed apoptosis (P = 0.027), and increased S phase cell numbers (P = 0.0036) in primary cultures of GCs, compared to the cells treated with a sequence scrambled control RNA oligonucleotide. This study unveiled the possible roles of three miRNAs in PCOS and might provide candidate biomarkers for PCOS diagnosis while in vivo functional studies, using transgenic or knockout mouse models, are expected to confirm the roles of dysregulated miRNAs in the pathogenesis of PCOS.

scholarly journals Levels of Apelin, Endoglin, and Transforming Growth Factor Beta 1 in Iraqi Women with Polycystic Ovary Syndrome

2020 ◽  
Vol 4 (1) ◽  
pp. 21-25
Author(s):  
Noor Alhuda K. Ibrahim ◽  
Wasnaa J. Mohammad ◽  
Sanan T. Abdawahab
Keyword(s):  
Growth Factor ◽  
Polycystic Ovary Syndrome ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Polycystic Ovary ◽  
Control Group ◽  
Model Assessment ◽  
Ovary Syndrome ◽  
Growth Factor Beta ◽  
Tgf Β1

Polycystic ovary syndrome (PCOS) is one of the most common causes of infertility in women of reproductive age. The aim of the study was to determine the level of apelin, insulin resistance (IR), transforming growth factor beta 1 (TGF-β1), and endoglin in women with polycystic ovary syndrome. Fifty PCOS patients and 40 non-PCOS infertile patients were recruited. The fasting serum levels of folliclestimulating hormone (FSH), luteinizing hormone (LH), testosterone (T), prolactin, fasting blood glucose, insulin, and apelin at the early follicular phase were measured. Levels of apelin, LH, LH/FSH, T, and fasting insulin, as well as homeostatic model assessment of IR (HOMA-IR) in PCOS patients, were significantly higher than in the control group. Correlation analysis showed that apelin level was positively correlated with body mass index and HOMA-IR. Apelin levels and TGF-β1 were significantly increased in PCOS patients while show decrease levels of endoglin.

Modulation of the Immune Response by Transforming Growth Factor Beta

1992 ◽  
Vol 99 (1) ◽  
pp. 1-7 ◽  
Author(s):  
A. Fontana ◽  
D.B. Constam ◽  
K. Frei ◽  
U. Malipiero ◽  
H.W. Pfister
Keyword(s):  
Immune Response ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Growth Factor Beta

scholarly journals Study the Effect of Interleukin36 Gamma and AMH in Iraqi Women with PCOS

2018 ◽  
Vol 28 (3) ◽  
pp. 151
Author(s):  
Wafa R. AlFatlawi
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Transforming Growth Factor ◽  
Seminal Fluid ◽  
Polycystic Ovary ◽  
Surrogate Marker ◽  
Reproductive Age ◽  
Endocrine Disorders ◽  
Ovary Syndrome ◽  
Markers Of Inflammation ◽  
Significant Difference

Polycystic ovary syndrome (PCOS) is one of the most common female endocrine disorders and affect approximately (5-10) % of women of reproductive age. Anti-Müllerian hormone (AMH) is a homodimeric glycoprotein, a member of the transforming growth factor-β superfamily, it is secreted exclusively from women by granulose cells of ovarian follicles and it is considered as the precise marker of follicle pool size. AMH has been shown to be a good surrogate marker for polycystic ovary syndrome (PCOS). Interleukins are considered as strong risk markers of inflammation. Interleukin-36 gamma (IL36) also known as interleukin-1 family member 9 (IL1F9) is a protein that in humans is encoded by the IL36G gene. Serum samples were collected on day 2 of the menstrual cycle. Serum IL36ɣ, FSH and LH concentration were measured by using ELISA. This study aimed to evaluate the association between IL36ɣ and AMH and study the relationship between obesity and AMH of women in the age of reproductive (25-35) yrs. This study included 28 infertile women with PCOS their husbands were apparently normal (hormones and seminal fluid analysis), their aged (25-35) years, and 20 healthy women aged (25-33) years as control. All control women & patients were from outpatients unit of Alkadumia teaching hospital at Baghdad and all the parameters were measured in Sigma Laboratory. Serum IL-36 ɣ elevated in PCOS patients mainly those with high AMH levels. This hormone increased in PCOS patients compared with control. There was a non-significant difference between patients and control to LH and FSH levels.

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