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Journal articles on the topic 'SGTA; androgen receptor; ovary'

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Published: 10 December 2022

Last updated: 29 January 2023

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1

Trotta, Andrew P., Eleanor F. Need, Lisa M. Butler, Luke A. Selth, Melissa A. O'Loughlin, Gerhard A. Coetzee, Wayne D. Tilley, and Grant Buchanan. "Subdomain structure of the co-chaperone SGTA and activity of its androgen receptor client." Journal of Molecular Endocrinology 49, no. 2 (June 12, 2012): 57–68. http://dx.doi.org/10.1530/jme-11-0152.

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Ligand-dependent activity of steroid receptors is affected by tetratricopeptide repeat (TPR)-containing co-chaperones, such as small glutamine-rich tetratricopeptide repeat-containing alpha (SGTA). However, the precise mechanisms by which the predominantly cytoplasmic TPR proteins affect downstream transcriptional outcomes of steroid signaling remain unclear. In this study, we assessed how SGTA affects ligand sensitivity and action of the androgen receptor (AR) using a transactivation profiling approach. Deletion mapping coupled with structural prediction, transcriptional assays, andin vivoregulation of AR-responsive promoters were used to assess the role of SGTA domains in AR responses. At subsaturating ligand concentrations of ≤0.1 nM 5α-dihydrotestosterone, SGTA overexpression constricted AR activity by an average of 32% (P<0.002) across the majority of androgen-responsive loci tested, as well as on endogenous promotersin vivo. The strength of the SGTA effect was associated with the presence or absence of bioinformatically predicated transcription factor motifs at each site. Homodimerizaion of SGTA, which is thought to be necessary for chaperone complex formation, was found to be dependent on the structural integrity of amino acids 1–80, and a core evolutionary conserved peptide within this region (amino acids 21–40) necessary for an effect of SGTA on the activity of both exogenous and endogenous AR. This study provides new insights into the subdomain structure of SGTA and how SGTA acts as a regulator of AR ligand sensitivity. A change in AR:SGTA ratio will impact the cellular and molecular response of prostate cancer cells to maintain androgenic signals, which may influence tumor progression.

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2

Tetsuka, M., P. F. Whitelaw, W. J. Bremner, M. R. Millar, C. D. Smyth, and S. G. Hillier. "Developmental regulation of androgen receptor in rat ovary." Journal of Endocrinology 145, no. 3 (June 1995): 535–43. http://dx.doi.org/10.1677/joe.0.1450535.

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Abstract Androgen receptor (AR) distribution and developmental regulation in the rat ovary were examined by semiquantitative immunohistochemistry. Ovarian AR mRNA levels were also determined by Northern analysis of total RNA and compared with the levels of cytochrome P450aromatase (P450arom), an established marker of preovulatory follicular maturity. Hypophysectomized immature female rats were treated with recombinant human (rh)-FSH and/or rh-LH, or human menopausal gonadotrophin (HMG). AR was predominately located in granulosa cells. There was no indication of specific AR immunoreactivity in thecal cells, but scattered stromal cells did stain positively. In control and LH-treated ovaries, only small preantral/early antral follicles were present. Granulosa cells in these follicles showed intense AR immunostaining. Treatment with FSH, FSH and LH or HMG stimulated varying degrees of preovulatory follicular development. In these follicles, the intensity of AR immunostaining progressively declined as follicular development progressed. In intact immature rats treated with FSH, the abundance of ovarian AR mRNA was significantly decreased to 35% of the control value while combined treatment of FSH and LH resulted in further down-regulation of AR mRNA expression to 17% of the control value. A decrease in the abundance of AR mRNA was accompanied by a simultaneous increase in the abundance of P450arom mRNA. Similar results were obtained in hypophysectomized immature rats treated with FSH and LH, suggesting an inverse relationship between AR mRNA expression and granulosa cell maturity. These results suggest that (1) the AR is most abundant in the granulosa cells of rat ovaries and (2) the expression of AR and its mRNA are developmentally regulated, being down-regulated during FSH-stimulated preovulatory follicular development. Journal of Endocrinology (1995) 145, 535–543

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3

Lin, Lawrence H., Maria C. P. Baracat, Gustavo A. R. Maciel, José M. Soares, and Edmund C. Baracat. "Androgen receptor gene polymorphism and polycystic ovary syndrome." International Journal of Gynecology & Obstetrics 120, no. 2 (November 24, 2012): 115–18. http://dx.doi.org/10.1016/j.ijgo.2012.08.016.

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4

Hampton, J. H., M. Manikkam, D. B. Lubahn, M. F. Smith, and H. A. Garverick. "Androgen receptor mRNA expression in the bovine ovary." Domestic Animal Endocrinology 27, no. 1 (July 2004): 81–88. http://dx.doi.org/10.1016/j.domaniend.2004.01.005.

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5

Salinas, Irving, Niharika Sinha, and Aritro Sen. "Androgen-induced epigenetic modulations in the ovary." Journal of Endocrinology 249, no. 3 (June 2021): R53—R64. http://dx.doi.org/10.1530/joe-20-0578.

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In recent years, androgens have emerged as critical regulators of female reproduction and women’s health in general. While high levels of androgens in women are associated with polycystic ovary syndrome (PCOS), recent evidence suggests that a certain amount of direct androgen action through androgen receptor is also essential for normal ovarian function. Moreover, prenatal androgen exposure has been reported to cause developmental reprogramming of the fetus that manifests into adult pathologies, supporting the Developmental Origins of Health and Disease (DOHaD) hypothesis. Therefore, it has become imperative to understand the underlying mechanism of androgen actions and its downstream effects under normal and pathophysiological conditions. Over the years, there has been a lot of studies on androgen receptor function as a transcriptional regulator in the nucleus as well as androgen-induced rapid extra-nuclear signaling. Conversely, new evidence suggests that androgen actions may also be mediated through epigenetic modulation involving both the nuclear and extra-nuclear androgen signaling. This review focuses on androgen-induced epigenetic modifications in female reproduction, specifically in the ovary, and discusses emerging concepts, latest perceptions, and highlight the areas that need further investigation.

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6

Abbott, David H. "Neuronal androgen receptor: Molecular gateway to polycystic ovary syndrome?" Proceedings of the National Academy of Sciences 114, no. 16 (April 4, 2017): 4045–47. http://dx.doi.org/10.1073/pnas.1703436114.

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7

Walters, Kirsty A. "Polycystic ovary syndrome: Is it androgen or estrogen receptor?" Current Opinion in Endocrine and Metabolic Research 12 (June 2020): 1–7. http://dx.doi.org/10.1016/j.coemr.2020.01.003.

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8

Duffy, Diane M., Salah E. Abdelgadir, Kenneth R. Stott, John A. Resko, Richard L. Stouffer, and Mary B. Zelinski-Wooten. "Androgen Receptor mRNA Expression in the Rhesus Monkey Ovary." Endocrine 11, no. 1 (1999): 23–30. http://dx.doi.org/10.1385/endo:11:1:23.

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9

Hirai, Mitsuo, Shuji Hirata, Takaaki Osada, Kazuki Hagihara, and Junzo Kato. "Androgen receptor mRNA in the rat ovary and uterus." Journal of Steroid Biochemistry and Molecular Biology 49, no. 1 (May 1994): 1–7. http://dx.doi.org/10.1016/0960-0760(94)90294-1.

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10

Wang, Fangfang, Jiexue Pan, Ye Liu, Qing Meng, Pingping Lv, Fan Qu, Guo-Lian Ding, et al. "Alternative splicing of the androgen receptor in polycystic ovary syndrome." Proceedings of the National Academy of Sciences 112, no. 15 (March 30, 2015): 4743–48. http://dx.doi.org/10.1073/pnas.1418216112.

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Polycystic ovary syndrome (PCOS) is one of the most common female endocrine disorders and a leading cause of female subfertility. The mechanism underlying the pathophysiology of PCOS remains to be illustrated. Here, we identify two alternative splice variants (ASVs) of the androgen receptor (AR), insertion and deletion isoforms, in granulosa cells (GCs) in ∼62% of patients with PCOS. AR ASVs are strongly associated with remarkable hyperandrogenism and abnormalities in folliculogenesis, and are absent from all control subjects without PCOS. Alternative splicing dramatically alters genome-wide AR recruitment and androgen-induced expression of genes related to androgen metabolism and folliculogenesis in human GCs. These findings establish alternative splicing of AR in GCs as the major pathogenic mechanism for hyperandrogenism and abnormal folliculogenesis in PCOS.

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11

Dai, Anyi, Guijun Yan, Qinyuan He, Yue Jiang, Qun Zhang, Ting Fang, Lijun Ding, Jianxin Sun, Haixiang Sun, and Yali Hu. "Orphan Nuclear Receptor Nur77 Regulates Androgen Receptor Gene Expression in Mouse Ovary." PLoS ONE 7, no. 6 (June 28, 2012): e39950. http://dx.doi.org/10.1371/journal.pone.0039950.

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12

Hillier, S. G., M. Tetsuka, and H. M. Fraser. "Location and developmental regulation of androgen receptor in primate ovary." Human Reproduction 12, no. 1 (January 1, 1997): 107–11. http://dx.doi.org/10.1093/humrep/12.1.107.

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13

GALAS, JERZY, MARIA SLOMCZYNSKA, and ANNA KWASNIK. "Androgen Receptor in the Ovary of Postnatal Bank Vole Females." Annals of the New York Academy of Sciences 1040, no. 1 (April 2005): 315–19. http://dx.doi.org/10.1196/annals.1327.050.

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14

Prizant, Hen, Norbert Gleicher, and Aritro Sen. "Androgen actions in the ovary: balance is key." Journal of Endocrinology 222, no. 3 (July 18, 2014): R141—R151. http://dx.doi.org/10.1530/joe-14-0296.

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For many decades, elevated androgens in women have been associated with poor reproductive health. However, recent studies have shown that androgens play a crucial role in women's fertility. The following review provides an overall perspective about how androgens and androgen receptor-mediated actions regulate normal follicular development, as well as discuss emerging concepts, latest perceptions, and controversies regarding androgen actions and signaling in the ovary.

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15

Yang, Mei, Jianhua Li, Yulin An, and Shuiwen Zhang. "Effects of androgen on immunohistochemical localization of androgen receptor and Connexin 43 in mouse ovary." Tissue and Cell 47, no. 5 (October 2015): 526–32. http://dx.doi.org/10.1016/j.tice.2015.06.003.

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16

Yongli, Chu, Sun Yongyu, and Qiu Hongyu. "Study of androgen and androgen receptor in relation to insulin resistance in polycystic ovary syndrome." Journal of Huazhong University of Science and Technology [Medical Sciences] 23, no. 1 (March 2003): 52–54. http://dx.doi.org/10.1007/bf02829462.

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17

McEwan, Iain J., Dagmara McGuinness, Colin W. Hay, Robert P. Millar, Philippa T. K. Saunders, and Hamish M. Fraser. "Identification of androgen receptor phosphorylation in the primate ovary in vivo." REPRODUCTION 140, no. 1 (July 2010): 93–104. http://dx.doi.org/10.1530/rep-10-0140.

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The androgen receptor (AR) is a member of the nuclear receptor superfamily, and is important for both male and female reproductive health. The receptor is a target for a number of post-translational modifications including phosphorylation, which has been intensively studied in vitro. However, little is known about the phosphorylation status of the receptor in target tissues in vivo. The common marmoset is a useful model for studying human reproductive functions, and comparison of the AR primary sequence from this primate shows high conservation of serines known to be phosphorylated in the human receptor and corresponding flanking amino acids. We have used a panel of phosphospecific antibodies to study AR phosphorylation in the marmoset ovary throughout the follicular phase and after treatment with GNRH antagonist or testosterone propionate. In normal follicular phase ovaries, total AR (both phosphorylated and non-phosphorylated forms) immunopositive staining was observed in several cell types including granulosa cells of developing follicles, theca cells and endothelial cells lining blood vessels. Receptor phosphorylation at serines 81, 308, and 650 was detected primarily in the granulosa cells of developing follicles, surface epithelium, and vessel endothelial cells. Testosterone treatment lead to a modest increase in AR staining in all stages of follicle studied, while GNRH antagonist had no effect. Neither treatment significantly altered the pattern of phosphorylation compared to the control group. These results demonstrate that phosphorylation of the AR occurs, at a subset of serine residues, in a reproductive target tissue in vivo, which appears refractory to hormonal manipulations.

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18

Shah, Nissar A., Heath J. Antoine, Marita Pall, Kent D. Taylor, Ricardo Azziz, and Mark O. Goodarzi. "Association of Androgen Receptor CAG Repeat Polymorphism and Polycystic Ovary Syndrome." Journal of Clinical Endocrinology & Metabolism 93, no. 5 (May 1, 2008): 1939–45. http://dx.doi.org/10.1210/jc.2008-0038.

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19

Meikle, A. W. "Association of Androgen Receptor CAG Repeat Polymorphism and Polycystic Ovary Syndrome." Yearbook of Endocrinology 2009 (January 2009): 237–38. http://dx.doi.org/10.1016/s0084-3741(08)79245-x.

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20

Walters, KirstyA, and DavidJ Handelsman. "Androgen receptor splice variants and polycystic ovary syndrome: cause or effect?" Asian Journal of Andrology 18, no. 3 (2016): 442. http://dx.doi.org/10.4103/1008-682x.161600.

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21

Astapova, Olga, Briaunna M. N. Minor, and Stephen R. Hammes. "Physiological and Pathological Androgen Actions in the Ovary." Endocrinology 160, no. 5 (March 26, 2019): 1166–74. http://dx.doi.org/10.1210/en.2019-00101.

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Abstract Androgens, although traditionally thought to be male sex steroids, play important roles in female reproduction, both in healthy and pathological states. This mini-review focuses on recent advances in our knowledge of the role of androgens in the ovary. Androgen receptor (AR) is expressed in oocytes, granulosa cells, and theca cells, and is temporally regulated during follicular development. Mouse knockout studies have shown that AR expression in granulosa cells is critical for normal follicular development and subsequent ovulation. In addition, androgens are involved in regulating dynamic changes in ovarian steroidogenesis that are critical for normal cycling. Androgen effects on follicle development have been incorporated into clinical practice in women with diminished ovarian reserve, albeit with limited success in available literature. At the other extreme, androgen excess leads to disordered follicle development and anovulatory infertility known as polycystic ovary syndrome (PCOS), with studies suggesting that theca cell AR may mediate many of these negative effects. Finally, both prenatal and postnatal animal models of androgen excess have been developed and are being used to study the pathophysiology of PCOS both within the ovary and with regard to overall metabolic health. Taken together, current scientific consensus is that a careful balance of androgen activity in the ovary is necessary for reproductive health in women.

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22

Yang, Jun-Ling, Chun-Ping Zhang, Lei Li, Lin Huang, Shao-Yang Ji, Cui-Ling Lu, Cui-Hong Fan, et al. "Testosterone Induces Redistribution of Forkhead Box-3a and Down-Regulation of Growth and Differentiation Factor 9 Messenger Ribonucleic Acid Expression at Early Stage of Mouse Folliculogenesis." Endocrinology 151, no. 2 (February 1, 2010): 774–82. http://dx.doi.org/10.1210/en.2009-0751.

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Increasing evidence has shown that excess androgen may be a main cause of polycystic ovary syndrome (PCOS). However, the molecular mechanism of androgen action on the ovary is unclear. To investigate the possible impacts of androgen on early follicular development, neonatal mouse ovaries mainly containing primordial follicles were cultured with testosterone. We demonstrated that the number of primary follicles was increased after 10 d culture with testosterone treatment via phosphatidylinositol 3-kinase/Akt pathway. Androgen induced Forkhead box (Foxo)-3a activation, and translocation of Foxo3a protein from oocyte nuclei to cytoplasm, which might be a key step for primordial follicle activation. Interestingly, testosterone was also capable of down-regulating growth and differentiation factor-9 expression via its receptor. In summary, we infer that intraovarian excess androgen in PCOS might result in excess early follicles by inducing oocyte Foxo3a translocation and follicular arrest by down-regulating growth and differentiation factor-9 expression.

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23

Jääskeläinen, Jarmo, Seija Korhonen, Raimo Voutilainen, Maritta Hippeläinen, and Seppo Heinonen. "Androgen receptor gene CAG length polymorphism in women with polycystic ovary syndrome." Fertility and Sterility 83, no. 6 (June 2005): 1724–28. http://dx.doi.org/10.1016/j.fertnstert.2004.11.080.

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24

FERK, P., M. PERME, N. TERAN, and K. GERSAK. "Androgen receptor gene (CAG)n polymorphism in patients with polycystic ovary syndrome." Fertility and Sterility 90, no. 3 (September 2008): 860–63. http://dx.doi.org/10.1016/j.fertnstert.2007.07.1291.

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25

Kim, Jin Ju, Seon Ha Choung, Young Min Choi, Sang Ho Yoon, Seok Hyun Kim, and Shin Yong Moon. "Androgen receptor gene CAG repeat polymorphism in women with polycystic ovary syndrome." Fertility and Sterility 90, no. 6 (December 2008): 2318–23. http://dx.doi.org/10.1016/j.fertnstert.2007.10.030.

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26

Hickey, T., A. Tuck, M. Butler, S. Jindal, T. Dodd, R. Norman, and W. Tilley. "415. Increased expression of an androgen receptor regulated gene, kit ligand, in polycystic ovaries." Reproduction, Fertility and Development 20, no. 9 (2008): 95. http://dx.doi.org/10.1071/srb08abs415.

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Polycystic ovaries (PCO) are induced by pathological or pharmacological female androgen excess, but the role of the androgen receptor (AR) in the pathogenesis of PCO is unknown. We therefore tested the hypothesis that PCO have increased expression of AR or kit ligand (KITL), a cytokine that was recently identified as a candidate AR-regulated gene in the ovary (1). Immunohistochemical analysis of AR and KITL expression was performed on archival paraffin-embedded sections of 8 morphologically normal and 8 polycystic ovaries from women under the age of 40 years. Stained sections were scanned with a NanoZoomer Digital Pathology System and immunoreactivity was qualitatively assessed using a 0-3+ scale, where 3+ represents the most intense staining. Electronic images of follicles at different stages of folliculogenesis were assessed by two independent observers who were blinded to the morphology of the source ovary. Each individual ovary contributed a minimum of 1 follicle per size class and a minimum of 10 follicles per size class were analysed. AR immunoreactivity was present in granulosa cells at all stages of folliculogenesis, in thecal cells of large antral follicles, and in the ovarian stroma. Staining intensity for AR did not differ between normal and polycystic ovaries. KITL expression, summarised in Table 1, was found to be significantly elevated in the oocytes of primordial and primary follicles and in the granulosa cells of follicles at all stages of folliculogenesis. These results show that AR expression is normal in PCO but expression of an AR-regulated gene is increased, potentially due to an excess of androgen hormone that is characteristic of women with PCO. Based on the roles of KITL established by murine studies, increased expression of KITL could explain many of the features of PCO including follicle excess, hyperthecosis and abnormal androgen secretion.

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27

Weil, S. J., K. Vendola, J. Zhou, O. O. Adesanya, J. Wang, J. Okafor, and C. A. Bondy. "Androgen Receptor Gene Expression in the Primate Ovary: Cellular Localization, Regulation, and Functional Correlations." Journal of Clinical Endocrinology & Metabolism 83, no. 7 (July 1, 1998): 2479–85. http://dx.doi.org/10.1210/jcem.83.7.4917.

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Excess androgens are associated with a characteristic polyfollicular ovarian morphology; however, it is not known to what extent this problem is due to direct androgen action on follicular development vs. interference with gonadotropin release at the level of the pituitary or hypothalamus. To elucidate potential androgen effects on the ovary, we investigated the cellular localization of androgen receptor (AR) messenger ribonucleic acid (mRNA) in rhesus monkey using in situ hybridization. To investigate the regulation of ovarian AR gene expression, we compared the relative abundance of AR transcripts in monkeys during follicular and luteal phases of the menstrual cycle and in monkeys treated with testosterone. To assess potential functional consequences of AR expression in the primate ovary, we compared AR mRNA levels with indexes of follicular cell proliferation and apoptosis in serial sections from individual follicles. AR mRNA expression was most abundant in granulosa cells of healthy preantral and antral follicles in the primate ovary. Theca interna and stromal cells also expressed AR mRNA, but to a lesser degree than granulosa cells. No significant cycle stage effects were noted in AR mRNA levels; however, larger numbers of animals would be necessary to definitively establish a cycle stage effect. AR mRNA level was significantly increased in granulosa cells and was decreased in theca interna and stromal cells of testosterone-treated monkeys. Importantly, granulosa cell AR mRNA abundance was positively correlated with expression of the proliferation-specific antigen Ki-67 (r = 0.91; P < 0.001) and negatively correlated with granulosa cell apoptosis (r = −0.64; P < 0.001). In summary, these data show that primate ovary AR gene expression is most abundant in granulosa cells of healthy growing follicles, where its expression is up-regulated by testosterone. The positive correlation between granulosa AR gene expression and cell proliferation and negative correlation with programmed cell death suggests that androgens stimulate early primate follicle development.

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28

Stener-Victorin, Elisabet, Maria Manti, Romina Fornes, Sanjiv Risal, Haojiang Lu, and Anna Benrick. "Origins and Impact of Psychological Traits in Polycystic Ovary Syndrome." Medical Sciences 7, no. 8 (August 5, 2019): 86. http://dx.doi.org/10.3390/medsci7080086.

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Women with polycystic ovary syndrome (PCOS) exhibit compromised psychiatric health. Independent of obesity, women with PCOS are more susceptible to have anxiety and depression diagnoses and other neuropsychiatric disorders. During pregnancy women with PCOS display high circulating androgen levels that may cause prenatal androgen exposure affecting the growing fetus and increasing the risk of mood disorders in offspring. Increasing evidence supports a non-genetic, maternal contribution to the development of PCOS and anxiety disorders in the next generation. Prenatal androgenized rodent models reflecting the anxiety-like phenotype of PCOS in the offspring, found evidence for the altered placenta and androgen receptor function in the amygdala, together with changes in the expression of genes associated with emotional regulation and steroid receptors in the amygdala and hippocampus. These findings defined a previously unknown mechanism that may be critical in understanding how maternal androgen excess can increase the risk of developing anxiety disorders in daughters and partly in sons of PCOS mothers. Maternal obesity is another common feature of PCOS causing an unfavorable intrauterine environment which may contribute to psychiatric problems in the offspring. Whether environmental factors such as prenatal androgen exposure and obesity increase the offspring’s susceptibility to develop psychiatric ill-health will be discussed.

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29

Torres Fernandez, Edgar D., Kristen V. Adams, Maryam Syed, Rodrigo O. Maranon, Damian G. Romero, and Licy L. Yanes Cardozo. "Long-Lasting Androgen-Induced Cardiometabolic Effects in Polycystic Ovary Syndrome." Journal of the Endocrine Society 2, no. 8 (July 10, 2018): 949–64. http://dx.doi.org/10.1210/js.2018-00131.

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Abstract Polycystic ovary syndrome (PCOS), the most common endocrine disorder in women of reproductive age, is characterized by androgen excess and ovarian dysfunction and presents with increased cardiometabolic risk factors such as obesity, insulin resistance, and elevated blood pressure (BP). We previously reported that administration of dihydrotestosterone (DHT) to female rats elicits cardiometabolic derangements similar to those found in women with PCOS. In this study, we tested the hypothesis that the DHT-mediated cardiometabolic derangements observed in PCOS are long lasting despite DHT withdrawal. Four-week-old female Sprague Dawley rats were treated with DHT (7.5 mg/90 days) or placebo for 6 months. DHT was discontinued (ex-DHT), and rats were followed for 6 additional months. After 6 months of DHT withdrawal, food intake, body weight, fat and lean mass, fasting plasma insulin, leptin, and adiponectin were elevated in ex-DHT rats. BP remained significantly elevated, and enalapril, an angiotensin-converting enzyme (ACE) inhibitor, normalized BP in ex-DHT rats. Expression of components of the intrarenal renin-angiotensin system was increased in ex-DHT rats. The cardiometabolic features found in ex-DHT rats were associated with lower plasma androgen levels but increased expression of renal and adipose tissue androgen receptors. In summary, androgen-induced cardiometabolic effects persisted after DHT withdrawal in a PCOS experimental model. Activation of intrarenal renin-angiotensin system plays a major role in the androgen-mediated increase in BP in ex-DHT. Upregulation of the renal and adipose tissue androgen receptor may explain the long-lasting effects of androgens. In clinical scenarios characterized by hyperandrogenemia in women, prompt normalization of androgen levels may be necessary to prevent their long-lasting cardiometabolic effects.

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30

Colina, Jose A., Katherine E. Zink, Kanella Eliadis, Reza Salehi, Emma S. Gargus, Sarah R. Wagner, Kristine J. Moss, et al. "Fallopian Tube-Derived Tumor Cells Induce Testosterone Secretion from the Ovary, Increasing Epithelial Proliferation and Invasion." Cancers 13, no. 8 (April 16, 2021): 1925. http://dx.doi.org/10.3390/cancers13081925.

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The fallopian tube epithelium is the site of origin for a majority of high grade serous ovarian carcinomas (HGSOC). The chemical communication between the fallopian tube and the ovary in the development of HGSOC from the fallopian tube is of interest since the fimbriated ends in proximity of the ovary harbor serous tubal intraepithelial carcinoma (STICs). Epidemiological data indicates that androgens play a role in ovarian carcinogenesis; however, the oncogenic impact of androgen exposure on the fallopian tube, or tubal neoplastic precursor lesions, has yet to be explored. In this report, imaging mass spectrometry identified that testosterone is produced by the ovary when exposed to tumorigenic fallopian tube derived PTEN deficient cells. Androgen exposure increased cellular viability, proliferation, and invasion of murine cell models of healthy fallopian tube epithelium and PAX2 deficient models of the preneoplastic secretory cell outgrowths (SCOUTs). Proliferation and invasion induced by androgen was reversed by co-treatment with androgen receptor (AR) antagonist, bicalutamide. Furthermore, ablation of phosphorylated ERK reversed proliferation, but not invasion. Investigation of two hyperandrogenic rodent models of polycystic ovarian syndrome revealed that peripheral administration of androgens does not induce fallopian proliferation in vivo. These data suggest that tumorigenic lesions in the fallopian tube may induce an androgenic microenvironment proximal to the ovary, which may in turn promote proliferation of the fallopian tube epithelium and preneoplastic lesions.

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31

Astapova, Olga, and Stephen R. Hammes. "Paxillin Is Required for Androgen Receptor Expression in Granulosa Cells." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A813—A814. http://dx.doi.org/10.1210/jendso/bvab048.1657.

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Abstract Androgens are important in female reproduction, as evident from studies of mouse ovary-specific androgen receptor knockout models characterized by sub-fertility and diminished ovarian reserve. Androgen activity specifically promotes granulosa cell proliferation and follicle progression. However, the molecular mechanisms mediating androgen activity in granulosa cells are unknown. Our lab previously showed that the cytoplasmic adaptor protein paxillin is required for full transcriptional activity by the androgen receptor (AR) in prostate cancer cells, therefore we examined how paxillin affects the androgen receptor in granulosa cells. We found that paxillin knockdown results in significantly reduced AR protein levels, independently of AR gene transcription in human granulosa-derived KGN cells. Similar to previous data from other cell types, we found that paxillin directly interacts with poly-A binding protein (PABP) in KGN cells using proximity ligation assay. Ligand binding further increases AR protein expression by reducing its degradation. Using immunofluorescence, we confirm that in both KGN and primary mouse granulosa cells, similarly to the prostate, ligand-bound AR is primarily localized in the nucleus. Based on this and previous studies, we propose that paxillin enhances AR mRNA translation through interaction with PABP, and ligand binding further increases AR protein level by nuclear retention, protecting from degradation in the cytoplasm. Our findings highlight a previously unrecognized role of paxillin in granulosa cells, where it may be an important target for modulating androgen activity in androgen-related disorders of female reproduction.

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32

Tian, Lifeng, Yang Zou, Jun Tan, Yaoqing Wang, Jia Chen, Leizhen Xia, Lixian Xu, Ge Chen, Qiongfang Wu, and Ouping Huang. "Androgen receptor gene mutations in 258 Han Chinese patients with polycystic ovary syndrome." Experimental and Therapeutic Medicine 21, no. 1 (November 11, 2020): 1. http://dx.doi.org/10.3892/etm.2020.9463.

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33

Peng, CY, XY Long, and GX Lu. "EL-001 Rs6152G/a polymorphism of androgen receptor gene and polycystic ovary syndrome." Reproductive BioMedicine Online 16 (January 2008): S—40—S—41. http://dx.doi.org/10.1016/s1472-6483(10)61567-2.

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34

Schüring, A., A. Welp, J. Gromoll, M. Zitzmann, B. Sonntag, E. Nieschlag, R. Greb, and L. Kiesel. "Role of the CAG Repeat Polymorphism of the Androgen Receptor Gene in Polycystic Ovary Syndrome (PCOS)." Experimental and Clinical Endocrinology & Diabetes 120, no. 02 (November 8, 2011): 73–79. http://dx.doi.org/10.1055/s-0031-1291343.

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AbstractPolycystic ovary syndrome (PCOS) is a frequent heterogenic disorder with a familial background. Androgenic effects, determining the clinical features of the syndrome, are mediated by the androgen receptor (AR), whose activity is modulated by a genetic polymorphism. We investigated the role of the CAG repeat polymorphism of the androgen receptor in PCOS.In the infertility unit of a university clinic, 72 PCOS patients were compared with 179 ovulatory controls undergoing a standardized diagnostic work-up. The number of CAG repeats was determined by PCR, labelling with IR-800 and PAGE. X-chromosome inactivation was assessed by a methylation-sensitive assay.Compared to controls, PCOS patients displayed a shorter mean CAG repeat length, encoding for higher AR activity (P=0.001). CAG repeat length correlated inversely with oligomenorrhea, a central androgen dependent feature of the syndrome (P=0.005). In a binomial regression analysis including BMI, LH and free testosterone, CAG repeat length was identified as an independent risk factor for PCOS (P=0.002).The CAG repeat polymorphism could constitute one of the genetic factors modulating the syndrome’s phenotype, contributing to its clinical heterogeneity and associated metabolic consequences.

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Rice, Suman, Kamal Ojha, Saffron Whitehead, and Helen Mason. "Stage-Specific Expression of Androgen Receptor, Follicle-Stimulating Hormone Receptor, and Anti-Müllerian Hormone Type II Receptor in Single, Isolated, Human Preantral Follicles: Relevance to Polycystic Ovaries." Journal of Clinical Endocrinology & Metabolism 92, no. 3 (March 1, 2007): 1034–40. http://dx.doi.org/10.1210/jc.2006-1697.

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Abstract Context: Recent evidence indicates that the increase in follicle numbers seen in polycystic ovary syndrome occurs early in folliculogenesis, with androgens being a likely causative candidate. In primates and sheep, androgen excess in utero results in ovarian changes similar to those in polycystic ovary syndrome. There is also increasing interest in the role of anti-Müllerian hormone (AMH) in early folliculogenesis because AMH knockout mice have an early depletion of their stock of primordial follicles. Initiation and early folliculogenesis may therefore be under negative control by AMH and positive control by androgens. Objective: Because AMH signals exclusively through its type II receptor (AMHRII), the aim of this study was to determine and colocalize the stage-specific expression of AMHRII, androgen receptor (AR), and FSH receptor (FSHR) mRNA in individual, well-characterized preantral follicles. Method: Follicles were isolated from human ovarian cortex obtained from either oophorectomies or cortical biopsies at cesarean section. Expression of AR, FSHR, and AMHRII mRNA was determined using a nested RT-PCR protocol. Results: AR mRNA was not detected in any primordial follicles but was from the transitional stage onward. The number of AR-positive follicles increased at each progressive growth stage. The expression of AR preceded that of FSHR, and only a small percentage of primary follicles expressed FSHR. AMHRII expression was rarely detected. Conclusions: This is the first study to identify the expression of AR in human transitional follicles. Results suggest a role for androgens in promoting early follicle growth and challenging the hypothesis that AMH exerts a direct, inhibitory effect on follicles at this stage.

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Tejura, S., G. R. Rodgers, M. H. Dunion, M. A. Parsons, J. C. E. Underwood, and P. M. Ingleton. "Sex-steroid receptors in the diethylnitrosamine model of hepatocarcinogenesis: modifications by gonadal ablation and steroid replacement therapy." Journal of Molecular Endocrinology 3, no. 3 (November 1989): 229–37. http://dx.doi.org/10.1677/jme.0.0030229.

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ABSTRACT The results of this study confirm our previous report of increased androgen receptor expression in livers of female SUAH Wistar rats during development of liver tumours induced by diethylnitrosamine (DENA). In adult female rats not treated with DENA, removal of the ovary increased liver androgen receptor levels but testosterone did not further enhance the androgen receptor status of ovariectomized rats. In normal adult males the testis and/or testosterone maintained high levels of androgen receptors but oestrogen reduced them in castrated rats. Oestrogen receptor levels were not significantly changed in either males or females by gonadectomy. Treatment of female rats with DENA for 10 and 16 weeks increased liver androgen receptors but oestrogen receptors were only reduced by 16 weeks of DENA treatment, whether the rats were intact or ovariectomized. Concentrations of liver androgen receptors were increased in intact and castrated male rats by 10 and 16 weeks of DENA treatment, an increase not seen in the previous experiments. Oestrogen appeared to inhibit both the increases in liver androgen receptor expression and liver tumour development in rats treated with the weakly carcinogenic dose of 10 weeks of DENA. However, the full carcinogenic dose of 16 weeks of DENA increased liver androgen receptors and decreased oestrogen receptors in female rats regardless of sex-steroid status. Development of malignant hepatocellular carcinoma (HCC) was associated with both an increase in liver androgen receptors and a decrease in oestrogen receptors. Maintenance of relatively high levels of liver oestrogen receptors appeared to protect the liver against development of HCC.

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Kato, Yuiko, Kazuhiko Ochiai, Masaki Michishita, Daigo Azakami, Rei Nakahira, Masami Morimatsu, Toshina Ishiguro-Oonuma, et al. "Molecular cloning of canine co-chaperone small glutamine-rich tetratricopeptide repeat-containing protein α (SGTA) and investigation of its ability to suppress androgen receptor signalling in androgen-independent prostate cancer." Veterinary Journal 206, no. 2 (November 2015): 143–48. http://dx.doi.org/10.1016/j.tvjl.2015.08.002.

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Liu, Zhenteng, Cuifang Hao, Dehua Song, Ning Zhang, Hongchu Bao, and Qinglan Qu. "Androgen Receptor Coregulator CTBP1-AS Is Associated With Polycystic Ovary Syndrome in Chinese Women." Reproductive Sciences 22, no. 7 (December 31, 2014): 829–37. http://dx.doi.org/10.1177/1933719114565037.

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Liu, Qiaorui, Jie Hong, Bin Cui, Yifei Zhang, Weiqiong Gu, Zhenni Chi, Yuxia Su, and Guang Ning. "Androgen receptor gene CAGn trinucleotide repeats polymorphism in Chinese women with polycystic ovary syndrome." Endocrine 33, no. 2 (April 2008): 165–70. http://dx.doi.org/10.1007/s12020-008-9069-7.

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Hogg, Kirsten, Alan S. McNeilly, and W. Colin Duncan. "Prenatal Androgen Exposure Leads to Alterations in Gene and Protein Expression in the Ovine Fetal Ovary." Endocrinology 152, no. 5 (February 15, 2011): 2048–59. http://dx.doi.org/10.1210/en.2010-1219.

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Exposure of a female fetus to increased androgens in utero results in an adult phenotype reminiscent of polycystic ovary syndrome. We investigated whether prenatal androgens could directly alter the structure and function of the fetal ovary. We examined fetal ovarian cell proliferation, germ cell volume, and the expression of steroid receptors and steroidogenic enzymes. In addition, we studied the inhibitors of differentiation (Ids) and the SLIT/Roundabout developmental pathways. Female fetuses were collected from ewes treated with 100 mg testosterone propionate (TP) or vehicle control (C), twice weekly from d 60 to 70 (C = 3, TP = 6) or d 90 (C = 6, TP = 8). Female fetuses were also collected at d 70 after a single injection of TP (20 mg) or vehicle C into the fetal flank at d 60 (C = 4, TP = 8). Prenatal androgenization had no effect on fetal ovarian morphology, cell proliferation, or germ cell volume. However, there was a reduction in the expression of StAR, CYP11A, CYP17, and LHR at d 90 of gestation. There was also an increase in Id1 immunostaining at d 90 and an increase in Id3 immunostaining at d 70. Direct injection of TP into the fetus down-regulated ovarian CYP11A, estrogen receptor α and β mRNA, and ROBO1 and up-regulated CYP19, androgen receptor immunostaining, and Id3 mRNA and protein. Although at d 90 prenatal androgenization does not result in structural changes of the fetal ovary, there are functional changes that may impact on ovarian development. TP has direct actions on the fetal ovary, and these may contribute to the adult ovarian phenotype in the ovine model of polycystic ovary syndrome.

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Wimmers, K., N. Trakooljul, K. Schellander, and S. Ponsuksili. "Polymorphisms of the androgen receptor gene associate with fatness, uterus and ovary measurements in the pig." Archives Animal Breeding 48, no. 4 (October 10, 2005): 372–82. http://dx.doi.org/10.5194/aab-48-372-2005.

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Abstract. Quantitative trait loci, QTL, for fatness and carcass traits in pigs have been recently mapped to the X chromosome approximately at the position where the androgen receptor gene (AR) is localized. The AR acts as a nuclear transcription factor regulating expression of a number of androgenic response genes during various stages of sexual development. The present study aimed to analyze association of the AR genotype on traits related to fatness and phenotype of primary female sexual organs, ovary and uterus. Animals of a F2 resource population based on Duroc and Berlin Miniature pig were genotyped at a multi-allelic microsatellite marker (CCTTT)n situated in the 5' untranslated region and a bi-allelic CAG-insertion/deletion polymorphism (CAG-INDEL) within exon 1 of the AR. Association analysis showed that the AR genotype both at the CAG-INDEL and microsatellite affect almost all fatness traits measured. The D allele inherited from Duroc was associated with the decrease of fat thickness. The AR genotypes also affect uterus and ovary measurements. The pigs homozygous for D allele were likely to have a lighter uterus, shorter uterus horns, oviducts and smaller ovaries than pigs homozygous for the M allele. Our results confirm the previously reported QTL for fatness traits and provide evidence for a QTL affecting dimensions of uterus and ovary on the X chromosome. The AR is a positional functional candidate gene for both trait complexes.

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Nam, Hyoun, Chung-Hoon Kim, Min-Young Cha, Jae-Min Kim, Byung-Moon Kang, and Han-Wook Yoo. "Polycystic ovary syndrome woman with heterozygous androgen receptor gene mutation who gave birth to a child with androgen insensitivity syndrome." Obstetrics & Gynecology Science 58, no. 2 (2015): 179. http://dx.doi.org/10.5468/ogs.2015.58.2.179.

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Martinez-Pinto, J., B. Piquer, M. Tiszavari, and H. E. Lara. "Neonatal exposure to estradiol valerate reprograms the rat ovary androgen receptor and anti-Müllerian hormone to a polycystic ovary phenotype." Reproductive Toxicology 75 (January 2018): 127–35. http://dx.doi.org/10.1016/j.reprotox.2017.10.005.

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Rodriguez Paris, Valentina, and Michael J. Bertoldo. "The Mechanism of Androgen Actions in PCOS Etiology." Medical Sciences 7, no. 9 (August 28, 2019): 89. http://dx.doi.org/10.3390/medsci7090089.

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Polycystic ovary syndrome (PCOS) is the most common endocrine condition in reproductive-age women. By comprising reproductive, endocrine, metabolic and psychological features—the cause of PCOS is still unknown. Consequently, there is no cure, and management is persistently suboptimal as it depends on the ad hoc management of symptoms only. Recently it has been revealed that androgens have an important role in regulating female fertility. Androgen actions are facilitated via the androgen receptor (AR) and transgenic Ar knockout mouse models have established that AR-mediated androgen actions have a part in regulating female fertility and ovarian function. Considerable evidence from human and animal studies currently reinforces the hypothesis that androgens in excess, working via the AR, play a key role in the origins of polycystic ovary syndrome (PCOS). Identifying and confirming the locations of AR-mediated actions and the molecular mechanisms involved in the development of PCOS is critical to provide the knowledge required for the future development of innovative, mechanism-based interventions for the treatment of PCOS. This review summarises fundamental scientific discoveries that have improved our knowledge of androgen actions in PCOS etiology and how this may form the future development of effective methods to reduce symptoms in patients with PCOS.

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Yazawa, Takashi, Miki Uesaka, Yoshihiko Inaoka, Tetsuya Mizutani, Toshio Sekiguchi, Takashi Kajitani, Takeshi Kitano, Akihiro Umezawa, and Kaoru Miyamoto. "Cyp11b1 Is Induced in the Murine Gonad by Luteinizing Hormone/Human Chorionic Gonadotropin and Involved in the Production of 11-Ketotestosterone, a Major Fish Androgen: Conservation and Evolution of the Androgen Metabolic Pathway." Endocrinology 149, no. 4 (December 27, 2007): 1786–92. http://dx.doi.org/10.1210/en.2007-1015.

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We have shown previously that Cyp11b1, an 11β-hydroxylase responsible for glucocorticoid biosynthesis in the adrenal gland, was induced by cAMP in androgen-producing Leydig-like cells derived from mesenchymal stem cells. We found that Cyp11b1 was induced in male Leydig cells, or female theca cells, when human chorionic gonadotropin was administered in immature mice. Expression of Cyp11b1 in rodent gonads caused the production of 11-ketotestosterone (11-KT), a major fish androgen, which induces male differentiation or spermatogenesis in fish. As in teleosts, plasma concentrations of 11-KT were elevated in human chorionic gonadotropin-treated mice. In contrast to teleosts, however, plasma concentrations of 11-KT were similar in both sexes, despite levels of testosterone, a precursor substrate, being about 20 times higher in male mice. Because expression of 11β-hydroxysteroid dehydrogenase type 2, was much higher in the mouse ovary than in the testis, conversion of testosterone into 11-KT may occur more efficiently in the ovary. In a luciferase reporter system that was responsive to and activated by androgens, 11-KT efficiently activated mammalian androgen receptor-mediated transactivation. Our results suggest that the androgen metabolic pathway is conserved between teleosts and mammals, despite sexual dominance and reproductive functions of 11-KT being altered during evolution.

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Van Nieuwerburgh, Filip, Dominic Stoop, Patrick Cabri, Marc Dhont, Dieter Deforce, and Petra De Sutter. "Shorter CAG repeats in the androgen receptor gene may enhance hyperandrogenicity in polycystic ovary syndrome." Gynecological Endocrinology 24, no. 12 (January 2008): 669–73. http://dx.doi.org/10.1080/09513590802342841.

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Lerner, Avi, Drashti Kewada, Ayan Ahmed, Kate Hardy, Mark Christian, and Stephen Franks. "Androgen Reduces Mitochondrial Respiration in Mouse Brown Adipocytes: A Model for Disordered Energy Balance in Polycystic Ovary Syndrome." International Journal of Molecular Sciences 22, no. 1 (December 29, 2020): 243. http://dx.doi.org/10.3390/ijms22010243.

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Polycystic ovary syndrome (PCOS) is a common endocrinopathy that is associated with an adverse metabolic profile including reduced postprandial thermogenesis. Although abnormalities in adipose tissue function have been widely reported in women with PCOS, less is known about direct effects of androgen on white and, particularly, brown adipocytes. The purpose of this study was to investigate the effect of the nonaromatizable androgen dihydrotestosterone (DHT) on (1) lipid accumulation and expression of adipogenic markers in immortalized mouse brown adipose cell lines (IMBATs), (2) mitochondrial respiration in IMBATs, (3) mitochondrial DNA content and gene expression, (4) expression of brown adipose tissue (BAT) markers and thermogenic activation. In addition, we profiled the relative levels of 38 adipokines secreted from BAT explants and looked at androgen effects on adipokine gene expression in both IMBATs and immortalized mouse white adipose (IMWATs) cell lines. Androgen treatment inhibited IMBAT differentiation in a dose-dependent manner, reduced markers of adipogenesis, and attenuated the β-adrenoceptor-stimulated increase in uncoupling protein-1 (UCP1) expression. In explants of mouse interscapular BAT, androgen reduced expression of UCP1, peroxisome proliferator-activated receptor-γ coactivator-1 (PCG-1) and Cidea. Significantly, as well as affecting genes involved in thermogenesis in BAT, androgen treatment reduced mitochondrial respiration in IMBATs, as measured by the Seahorse XF method. The results of this study suggest a role for excess androgen in inhibiting brown adipogenesis, attenuating the activation of thermogenesis and reducing mitochondrial respiration in BAT. Together, these data provide a plausible molecular mechanism that may contribute to reduced postprandial thermogenesis and the tendency to obesity in women with PCOS.

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Orisaka, Makoto, Katsushige Hattori, Shin Fukuda, Tetsuya Mizutani, Kaoru Miyamoto, Takashi Sato, Benjamin K. Tsang, Fumikazu Kotsuji, and Yoshio Yoshida. "Dysregulation of Ovarian Follicular Development in Female Rat: LH Decreases FSH Sensitivity During Preantral-Early Antral Transition." Endocrinology 154, no. 8 (August 1, 2013): 2870–80. http://dx.doi.org/10.1210/en.2012-2173.

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Abstract Several clinical studies have shown a correlation of hypersecretion of LH and polycystic ovary syndrome (PCOS), infertility, and miscarriage in women, suggesting that chronically elevated LH impairs fertility. Growth arrest of small antral follicles in PCOS is also assumed to be associated with an abnormal endocrine environment involving increased LH stimulation, a hyperandrogenic milieu, and subsequent dysregulated FSH action in the ovarian follicles. In this study, we examined whether and how LH modulates follicular development and steroid production during preantral-early antral follicle transition by using a rat preantral follicle culture system. LH augments testosterone and estradiol production in preantral follicles via up-regulating mRNA abundance of CYP17A1 and CYP19A1. LH promotes rat preantral follicle growth, and the follicular size reaches that of early antral follicles in vitro, a response attenuated by the specific androgen receptor antagonist and a targeted disruption of androgen receptor gene. Sustained follicle stimulation by LH, but not by androgen, decreases FSH receptor mRNA levels and FSH receptor signaling and inhibits FSH-induced follicular growth. The data suggest that LH promotes preantral-early antral transition via the increased synthesis and growth-promoting action of androgen. However, chronic LH stimulation impairs FSH-dependent antral follicle growth by suppressing granulosa cell FSHR expression via the modulation of intraovarian regulators, including LH-induced thecal factors.

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Cárdenas, H., and W. F. Pope. "Androgen receptor and follicle-stimulating hormone receptor in the pig ovary during the follicular phase of the estrous cycle*." Molecular Reproduction and Development 62, no. 1 (March 18, 2002): 92–98. http://dx.doi.org/10.1002/mrd.10060.

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Caldwell, Aimee S. L., Melissa C. Edwards, Reena Desai, Mark Jimenez, Robert B. Gilchrist, David J. Handelsman, and Kirsty A. Walters. "Neuroendocrine androgen action is a key extraovarian mediator in the development of polycystic ovary syndrome." Proceedings of the National Academy of Sciences 114, no. 16 (March 20, 2017): E3334—E3343. http://dx.doi.org/10.1073/pnas.1616467114.

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Polycystic ovary syndrome (PCOS) is a complex hormonal disorder characterized by reproductive, endocrine, and metabolic abnormalities. As the origins of PCOS remain unknown, mechanism-based treatments are not feasible and current management relies on treatment of symptoms. Hyperandrogenism is the most consistent PCOS characteristic; however, it is unclear whether androgen excess, which is treatable, is a cause or a consequence of PCOS. As androgens mediate their actions via the androgen receptor (AR), we combined a mouse model of dihydrotestosterone (DHT)-induced PCOS with global and cell-specific AR-resistant (ARKO) mice to investigate the locus of androgen actions that mediate the development of the PCOS phenotype. Global loss of the AR reveals that AR signaling is required for all DHT-induced features of PCOS. Neuron-specific AR signaling was required for the development of dysfunctional ovulation, classic polycystic ovaries, reduced large antral follicle health, and several metabolic traits including obesity and dyslipidemia. In addition, ovariectomized ARKO hosts with wild-type ovary transplants displayed normal estrous cycles and corpora lutea, despite DHT treatment, implying extraovarian and not intraovarian AR actions are key loci of androgen action in generating the PCOS phenotype. These findings provide strong evidence that neuroendocrine genomic AR signaling is an important extraovarian mediator in the development of PCOS traits. Thus, targeting AR-driven mechanisms that initiate PCOS is a promising strategy for the development of novel treatments for PCOS.

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