scholarly journals Levels of sex steroid hormones and their receptors in women with preeclampsia

2020 ◽  
Author(s):  
Kuo-Chung Lan(Former Corresponding Author) ◽  
Yun-Ju Lai ◽  
Hsin-Hsin Cheng ◽  
Ni-Chin Tsai ◽  
Yu-Ting Su ◽  
...  

Abstract Background: Pregnant women have high serum concentrations of sex steroid hormones, which are major regulators of paracrine and autocrine responses for many maternal and placental functions. The main purpose of this study was to compare patients with preeclampsia and patients with uncomplicated pregnancies in terms of serum steroid hormones (estradiol [E2], progesterone [P4], dehydroepiandrosterone sulfate [DHEAS], and testosterone [T]) throughout pregnancy and the levels of cord blood and placental steroid receptors during the third trimester. Methods: Quantitative real-time reverse transcription PCR, western blotting, and immunohistochemistry were used to determine the levels of steroid hormones in the serum and cord blood and the placental levels of estrogen receptor-α (ERα), ERβ, androgen receptor (AR), and progesterone receptor (PR). Results: There were 45 women in the uncomplicated pregnancy group and 30 women in the preeclampsia group. Serum levels of T were greater and serum levels of E2 were reduced in the preeclampsia group, but the two groups had similar levels of P4 and DHEAS during the third trimester. Cord blood had a decreased level of DHEAS in the preeclampsia group, but the two groups had similar levels of P4, E2, and T. The two groups had similar placental mRNA levels of ERα, ERβ, AR, and PR, but the preeclampsia group had a higher level of ERβ protein and a lower level of ERα protein. Immunohistochemistry indicated that the preeclampsia group had a greater level of ERβ in the nucleus and cytoplasm of syncytiotrophoblasts and stromal cells. Conclusions: Women with preeclampsia had lower levels of steroid hormones, estrogen, and ERα but higher levels of T and ERβ. These molecules may have roles in the pathogenesis of preeclampsia.

2019 ◽  
Author(s):  
Kuo-Chung Lan ◽  
Yun-Ju Lai ◽  
Hsin-Hsin Cheng ◽  
Ni-Chin Tsai ◽  
Yu-Ting Su ◽  
...  

Abstract Background: Pregnant women have high serum concentrations of sex steroid hormones, which are major regulators of paracrine and autocrine responses for many maternal and placental functions. The main purpose of this study is to compare patients with preeclampsia and patients with uncomplicated pregnancies in terms of serum of steroid hormones (estradiol [E2), progesterone [P4), dehydroepiandrosterone sulfate [DHEAS), and testosterone [T)) throughout pregnancy, and the levels of cord blood and placental steroid receptors during the third trimester. Methods: Quantitative real-time reverse transcription PCR, western blotting, and immunohistochemistry were used to determine the levels of steroid hormones in the serum and cord blood, and the placental levels of estrogen receptor-α (ERα), ERβ, androgen receptor (AR), and progesterone receptor (PR). Results: There were 45 women in the uncomplicated pregnancy group and 30 women in the preeclampsia group. Serum levels of T were greater and serum levels of E2 were reduced in the preeclampsia group, but the two groups had similar levels of P4 and DHEAS during the third trimester. Cord blood had a decreased level of DHEAS in the preeclampsia group, but the two groups had similar levels of P4, E2, and T. The two groups had similar placental mRNA levels of ERα, ERβ, AR, and PR, but the preeclampsia group had a higher level of ERβ protein and a lower level of ERα protein. Immunohistochemistry indicated the preeclampsia group had a greater level of ERβ in the nucleus and cytoplasm of syncytiotrophoblasts and stromal cells. Conclusions: Women with preeclampsia had lower levels of steroid hormones, estrogen, and ERα, but higher levels of T and ERβ. These molecules may have roles in the pathogenesis of preeclampsia.


2010 ◽  
Vol 28 (15_suppl) ◽  
pp. e21097-e21097
Author(s):  
M. Á. Berciano Guerrero ◽  
J. De la Haba Rodriguez ◽  
J. Castellano ◽  
I. Porras ◽  
G. Pulido ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2588
Author(s):  
Naoko Honma ◽  
Yoko Matsuda ◽  
Tetuo Mikami

Triple-negative breast cancer (TNBC) lacks an effective treatment target and is usually associated with a poor clinical outcome; however, hormone unresponsiveness, which is the most important biological characteristic of TNBC, only means the lack of nuclear estrogenic signaling through the classical estrogen receptor (ER), ER-α. Several sex steroid receptors other than ER-α: androgen receptor (AR), second ER, ER-β, and non-nuclear receptors represented by G-protein-coupled estrogen receptor (GPER), are frequently expressed in TNBC and their biological and clinical importance has been suggested by a large number of studies. Despite the structural similarity between each sex steroid hormone (androgens and estrogens) or each receptor (AR and ER-β), and similarity in the signaling mechanisms of these hormones, most studies or reviews focused on one of these receptors, and rarely reviewed them in a comprehensive way. Considering the coexistence of these hormones and their receptors in TNBC in a clinical setting, a comprehensive viewpoint would be important to correctly understand the association between the carcinogenic mechanism or pathobiology of TNBC and sex steroid hormones. In this review, the carcinogenic or pathobiological role of sex steroid hormones in TNBC is considered, focusing on the common and divergent features of the action of these hormones.


2012 ◽  
Vol 23 (3) ◽  
pp. 445-454 ◽  
Author(s):  
Tanya Agurs-Collins ◽  
Sabine Rohrmann ◽  
Catherine Sutcliffe ◽  
Jessica L. Bienstock ◽  
Deborah Monsegue ◽  
...  

2012 ◽  
Vol 15 (4) ◽  
pp. 208-215 ◽  
Author(s):  
Monika Eichholzer ◽  
Aline Barbir ◽  
Shehzad Basaria ◽  
Adrian S. Dobs ◽  
Manning Feinleib ◽  
...  

2020 ◽  
Vol 245 (2) ◽  
pp. 301-314
Author(s):  
Maria Konstandi ◽  
Christina E Andriopoulou ◽  
Jie Cheng ◽  
Frank J Gonzalez

The CYP2D subfamily catalyses the metabolism of about 25% of prescribed drugs, including the majority of antidepressants and antipsychotics. At present, the mechanism of hepatic CYP2D regulation remains largely unknown. This study investigated the role of sex steroid hormones in CYP2D regulation. For this purpose, Cyp2d22 expression was assessed in the distinct phases of the estrous cycle of normocyclic C57BL/6J (WT) female mice. Cyp2d22 was also evaluated in ovariectomised WT and CYP2D6-humanized (hCYP2D6) mice that received hormonal supplementation with either 17β-estradiol (E2) and/or progesterone. Comparisons were also made to male mice. The data revealed that hepatic Cyp2d22 mRNA, protein and activity levels were higher at estrous compared to the other phases of the estrous cycle and that ovariectomy repressed Cyp2d22 expression in WT mice. Tamoxifen, an anti-estrogenic compound, also repressed hepatic Cyp2d22 via activation of GH/STAT5b and PI3k/AKT signaling pathways. Both hormones prevented the ovariectomy-mediated Cyp2d22 repression. In case of progesterone, this may be mediated by inhibition of the PI3k/AKT/FOX01 pathway. Notably, Cyp2d22 mRNA levels in WT males were similar to those in ovariectomised mice and were markedly lower compared to females at estrous, a differentiation potentially regulated by the GH/STAT5b pathway. Sex steroid hormone-related alterations in Cyp2d22 mRNA expression were highly correlated with Hnf1a mRNA. Interestingly, fluctuations in Cyp2d22 in hippocampus and cerebellum followed those in liver. In contrast to WT mice, ovariectomy induced hepatic CYP2D6 expression in hCYP2D6 mice, whereas E2 and/or progesterone prevented this induction. Apparently, sex steroid hormones display a significant gender- and species-specific role in the regulation of CYP2D.


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