Free and Protein-Bound Plasma Estradiol-17β During the Menstrual Cycle

Wu, Chung Hsuen; Motohashi, Toru; Abdel-Rahman, H; Flickinger, George L.; Mikhail, George R.

doi:10.1210/jcem-43-2-436

Cited by 84 publications

(25 citation statements)

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“…The proportion of free and bound cortisol was measured in un diluted serum and CSF by equilibrium dialysis [35]. Samples of se rum and CSF taken from each animal in experiment 2 were pooled according to treatment and lime of sample.…”

Section: Measurement O F Free and Bound Cortisolmentioning

confidence: 99%

Factors Regulating Levels of Cortisol in Cerebrospinal Fluid of Monkeys during Acute and Chronic Hypercortisolemia

Martensz¹,

Herbert²,

Stacey³

1983

Neuroendocrinology

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Cortisol levels in the serum and cerebrospinal fluid (CSF) were studied in ovariectomized, estrogen-treated monkeys during either prolonged hypercortisolemia or the more transient effects of a bolus injection of cortisol. Control (saline-treated) animals showed the expected diurnal rhythm in serum cortisol, but proportionately more cortisol was present in the CSF when serum levels were high (i.e. in the morning). Prolonged hypercortisolemia for up to 37 days was produced by either thrice daily injections of cortisol itself or single daily injections of ACTH_1-24 in the morning. Both treatments produced disproportionately larger amounts of cortisol in the CSF than in the serum, and the CSF/serum cortisol ratio was increased. Furthermore, prolonged ACTH treatment caused a marked elevation in CSF cortisol in afternoon samples taken at 16.30 h compared with those at 10.00 h, in the absence of a similar change in serum cortisol levels. The relative importance of entry and clearance of cortisol in the CSF in these conditions was studied in several ways. ‘Free’ cortisol levels in serum (determined by equilibrium dialysis) were equal to CSF cortisol levels in control monkeys, but were less than those in the CSF of hypercortisolemic animals. Entry of cortisol into CSF after a bolus injection was rapid, but, unlike serum, CSF cortisol levels did not decline significantly over a 70-min sampling period and the delayed clearance from the CSF could account for some of the effects seen during hypercortisolemia. Neither high levels of prolactin (which is elevated together with cortisol in ‘stress’), induced by giving sulpiride, nor treatment with progesterone (which is also bound by corticosteroid binding globulin) altered the distribution of cortisol between blood and CSF. The concentrations of cortisol in the CSF therefore are regulated by factors influencing both its entry and clearance from the cerebral compartment. Neural tissues sensitive to cortisol are thus exposed to levels of this hormone that are both qualitatively and quantitatively different from those expected by direct extrapolation from serum levels.

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Section: Measurement O F Free and Bound Cortisolmentioning

confidence: 99%

Factors Regulating Levels of Cortisol in Cerebrospinal Fluid of Monkeys during Acute and Chronic Hypercortisolemia

Martensz¹,

Herbert²,

Stacey³

1983

Neuroendocrinology

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“…In the present study, we found that E 2 could dose-dependently promote the migration of MCF-7 breast cancer cells via up-regulation of MRTF-A and its target genes, MYL9 and CYR61. In addition, these effects were dramatically increased when the concentration of E 2 was higher than 10 29 M. It was reported that the plasma concentration of serum estradiol typically fluctuates in a wide range of 1.7-7.5 Â 10 210 M in the normal menstrual cycle of adult female, and it always decreases to about 1.5-2.5 Â 10 211 M in postmenopausal women [16,17]. Therefore, our results suggested that the MRTF-A signal pathway could be markedly activated when the breast cancer cells were exposed to estrogen at higher physiological levels, and this event might contribute to the excessive estrogen-stimulated breast cancer metastasis.…”

Section: Discussionmentioning

confidence: 98%

Myocardin-related transcription factor A is up-regulated by 17β-estradiol and promotes migration of MCF-7 breast cancer cells via transactivation of <italic>MYL9</italic> and <italic>CYR61</italic>

Zhang¹,

Luo²,

Liu³

et al. 2013

ABBS

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Many lines of evidence have suggested that estrogen plays important roles not only in the initiation and proliferation of breast cancer, but also in cancer metastasis. However, the mechanistic basis of the latter events is poorly understood. In addition, recent studies have suggested that myocardin-related transcription factor A (MRTF-A) might be related to cancer metastasis. However, as reports are contradictory, certain of its roles still remain confusing. In the present study, we showed that excessive 17b-estradiol could promote the migration of MCF-7 breast cancer cells and up-regulate the expression of MRTF-A, myosin regulatory light chain 9 (MYL9), and cysteine-rich angiogenic inducer 61 (CYR61). Overexpression of MRTF-A significantly promoted the migration of MCF-7 cells through its transactivation effects on MYL9 and CYR61 genes, while RNA interference-mediated knockdown of MRTF-A strongly inhibited transcription and expression of the target genes and reduced the migration ability of MCF-7 cells. These results provided novel evidence supporting the metastasispromoting functions of MRTF-A, and implied that MRTF-A might be a switch for the estrogen pathway to change its proliferation-promoting roles into migration-stimulating roles in breast cancer.

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“…However, shorter halflife of testosterone than estrogen in women, and more affinity of SHBG to testosterone than to estrogen [10] might lead to the conclusion that low SHBG levels are more likely to cause hyperandrogenism in women.…”

Section: Discussionmentioning

confidence: 99%

Endocrine Features in Eutestosteronemic Women with Polycystic Ovaries

Wada

Imai²,

Itoh³

et al. 1994

Gynecol Obstet Invest

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We attempted to assess the association between hyperandrogenemia and inappropriate gonadotropin secretion in women with polycystic ovaries (PCO). Thirty-one patients diagnosed as PCO by ultrasonography were divided into two subgroups: 17 with high serum total testosterone (T) level ( > 0.5 ng/ml) and 14 with normal serum total T level ( < 0.5 ng/ml). Both subgroups presented for the complaints of oligomenorrhea and/or hirsutism. The control group consisted of 15 women with regular ovulation for reference data collection. The PCO subjects with normal T, but not those with high T, revealed remarkable depletion of sex hormone binding globulin (SHBG), as compared with control. The PCO subject groups with high and normal serum T did not differ with respect to estrogen level, androgen level, follicle-stimulating hormone and prolactin levels, and SHBG concentration. Solely serum luteinizing hor-mon (LH) level was observed to be higher in those with high T, as typical features, than another subgroup or control. These data suggest that an increase in bioactive T as a result of decrease in serum SHBG or LH elevation may contribute to ovarian dysfunction in the patient with PCO.

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Free and Protein-Bound Plasma Estradiol-17β During the Menstrual Cycle

Cited by 84 publications

References 0 publications

Factors Regulating Levels of Cortisol in Cerebrospinal Fluid of Monkeys during Acute and Chronic Hypercortisolemia

Factors Regulating Levels of Cortisol in Cerebrospinal Fluid of Monkeys during Acute and Chronic Hypercortisolemia

Myocardin-related transcription factor A is up-regulated by 17β-estradiol and promotes migration of MCF-7 breast cancer cells via transactivation of <italic>MYL9</italic> and <italic>CYR61</italic>

Endocrine Features in Eutestosteronemic Women with Polycystic Ovaries

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Free and Protein-Bound Plasma Estradiol-17β During the Menstrual Cycle

Cited by 84 publications

References 0 publications

Factors Regulating Levels of Cortisol in Cerebrospinal Fluid of Monkeys during Acute and Chronic Hypercortisolemia

Factors Regulating Levels of Cortisol in Cerebrospinal Fluid of Monkeys during Acute and Chronic Hypercortisolemia

Myocardin-related transcription factor A is up-regulated by 17&beta;-estradiol and promotes migration of MCF-7 breast cancer cells via transactivation of &lt;italic&gt;MYL9&lt;/italic&gt; and &lt;italic&gt;CYR61&lt;/italic&gt;

Endocrine Features in Eutestosteronemic Women with Polycystic Ovaries

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Myocardin-related transcription factor A is up-regulated by 17β-estradiol and promotes migration of MCF-7 breast cancer cells via transactivation of <italic>MYL9</italic> and <italic>CYR61</italic>