Sex hormone-binding globulin mRNA levels in human uterine endometrium

1994 ◽  
Vol 131 (6) ◽  
pp. 623-629 ◽  
Author(s):  
Ryou Misao ◽  
Naoki Itoh ◽  
Hidehiro Mori ◽  
Jiro Fujimoto ◽  
Teruhiko Tamaya

Misao R, Itoh N, Mori H, Fujimoto J, Tamaya T. Sex hormone-binding globulin mRNA levels in human uterine endometrium. Eur J Endocrinol 1994;131:623–9. ISSN 0804–4643 Sex hormone-binding globulin (SHBG) is a specific steroid hormone-binding protein that plays a role in transporting dihydrotestosterone, testosterone and estradiol-17β (E2), altering their concentration in blood and influencing their biological action. Recently it has been reported that immunoreactive SHBG is localized in target tissues and that SHBG mRNA was identified in human endometrial and prostatic cell lines. In the present work, SHBG mRNA was detected in human normal endometrial tissues using Northern blot analysis and polymerase chain reaction. Its level was higher (p < 0.02) in the secretory phase than in the proliferative phase. In the secretory phase, the endometrial SHBG mRNA level was correlated positively with serum E2 and progesterone level (p < 0.05). However, there was a negative correlation between endometrial SHBG mRNA level and serum E2 /progesterone ratio (p < 0.01). These findings suggest that SHBG is synthesized in the uterine endometrium and a part of its synthesis is regulated complexly by sex steroid hormones such as E2 and progesterone. Ryou Misao, Department of Obstetrics and Gynecology, Gifu University School of Medicine, Tsukasamachi-40. Gifu 500, Japan

1995 ◽  
Vol 133 (3) ◽  
pp. 327-334 ◽  
Author(s):  
Ryou Misao ◽  
Yoshihito Nakanishi ◽  
Jiro Fujimoto ◽  
Masashi Hori ◽  
Satoshi Ichigo ◽  
...  

Misao R, Nakanishi Y, Fujimoto J. Hori M, Ichigo S, Tamaya T. Expression of sex hormone-binding globulin mRNA in human ovarian cancers. Eur J Endocrinol 1995;133:327–34. ISSN 0804–4643 To know the role of sex hormone-binding globulin (SHBG) in the intracellular steroidal actions in human ovarian cancers, the expression of SHBG mRNA as a substitute for intracellular SHBG expression was investigated in normal ovarian tissues and ovarian tumors. In the present study, we used competitive reverse transcription–polymerase chain reaction–Southern blot analysis to evaluate SHBG mRNA levels. The expression of SHBG mRNA was detected in all normal ovaries and benign and malignant ovarian tumors analyzed. There were no significant differences in the mean SHBG mRNA levels among the three types of tissue. The expression in normal ovaries was significantly higher (p < 0.01) in premenopause, suggesting the predominance of a sex steroid hormone effect on ovarian SHBG synthesis. Relative overexpression of SHBG mRNA was observed in six out of 22 cases (27%) of ovarian cancer (three cases of endometrioid adenocarcinoma, two cases of serous cystadenocarcinoma and one case of mucinous cystadenocarcinoma) in comparison with normal ovaries and benign ovarian tumors. There was no difference in expression among the clinical stages of ovarian cancers. These data suggest that normal human ovaries and ovarian tumors might synthesize SHBG intracellularly, ovarian cancers might conserve an estrogen-associated property via SHBG and the regulation of intracellular SHBG expression might be changed in some cancers. Ryou Misao, Department of Obstetrics and Gynecology, Gifu University School of Medicine, 40 Tsukasamachi, Gifu 500, Japan


2009 ◽  
Vol 43 (1) ◽  
pp. 19-27 ◽  
Author(s):  
David M Selva ◽  
Geoffrey L Hammond

Thyroid hormones increase hepatic sex hormone-binding globulin (SHBG) production, which is also regulated by hepatocyte nuclear factor-4α (HNF-4α) in response to changes in the metabolic state of the liver. Since the human SHBG promoter lacks a typical thyroid hormone response element, and because thyroid hormones influence metabolic state, we set out to determine whether thyroid hormones mediate SHBG expression indirectly via changes in HNF-4α levels in HepG2 human hepatoblastoma cells, and in the livers of transgenic mice that express a 4.3 kb human SHBG transgene under the control of its own 0.8 kb promoter sequence. Thyroid hormones (triiodothyronine (T3) and thyroxine (T4)) increase SHBG accumulation in HepG2 cell culture medium over 5 days, and increase cellular SHBG mRNA levels. In addition, T4 treatment of HepG2 cells for 5 days increased HNF-4α mRNA and HNF-4α levels in concert with decreased cellular palmitate levels. Plasma SHBG levels were also increased in mice expressing a human SHBG transgene after 5 days treatment with T3 along with increased hepatic HNF-4α levels. In HepG2 cells, the human SHBG promoter failed to respond acutely (within 24 h) to T4 treatment, but a 4-day pre-treatment with T4 resulted in a robust response that was prevented by co-treatment with HNF-4α siRNA, or by blocking the β-oxidation of palmitate through co-treatment with the carnitine palmitoyltransferase I inhibitor, etomoxir. These data lead us to conclude that thyroid hormones increase SHBG production indirectly by increasing HNF-4α gene expression, and by reducing cellular palmitate levels that further contribute to increased HNF-4α levels in hepatocytes.


1982 ◽  
Vol 101 (2) ◽  
pp. 248-253 ◽  
Author(s):  
Viveca Odlind ◽  
Kerstin Elamsson ◽  
Doris E. Englund ◽  
Arne Victor ◽  
Elof D. B. Johansson

Abstract. Sex hormone binding globulin (SHBG) levels were studied for possible effects of oestradiol-17β on SHBG. No change in SHBG plasma was recorded during normal menstrual cycles or during treatment with oestradiol-17β to menopausal women. However, gonadotrophin treatment to amenorrhoeic women to induce ovulation resulted in high oestradiol concentrations and a pronounced increase in SHBG was found during the luteal phase of these cycles. A marked increase of SHBG was also recorded in a woman with pronounced fluctuations of oestradiol during treatment with levonorgestrel sc implants for contraception. In conclusion, effects on SHBG were only found when extraordinarily high levels of plasma oestradiol were recorded.


1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S144 ◽  
Author(s):  
G. SINNECKER ◽  
E. LUDWIG ◽  
A. KRENZ ◽  
R.P. WILLIG

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