The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

SureCN13481084     (17S)-13-methyl- 6,7,8,9,11,12,14,15,16,17...

Synonyms: AC1O3H5P, Estra-1,3,5(10)-triene-3,17-diol (17.beta.)-
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of estradiol

  • E2 (30 nM) caused, within 24 hr, a 70-200% increase in creatine kinase (CK; ATP:creatine N-phosphotransferase, EC specific activity in ROS 17/2.8 rat osteogenic sarcoma cells, MC3T3-E1 mouse calvaria-derived cells, and rat fetal calvaria cells, and a 40% increase in rat epiphyseal cartilage cells [1].
  • Susceptibility to drug-induced coronary vasospasm in rhesus monkeys increases after removal of the ovaries and can be normalized by adding back physiological levels of estradiol-17ss (E2) and/or natural progesterone (P) in vivo as reported recently by our group [2].
  • We hypothesize that vascular hyperreactivity, which may be a critical factor involved in the increased incidence of coronary artery vasospasm and ischemic heart disease in postmenopausal women, can be normalized by E2 and/or P through direct actions on coronary artery vascular muscle cells [2].
  • To test this hypothesis we have introduced eukaryotic expression vectors directing the expression of TGF-alpha mRNA into E2-responsive MCF-7 human breast cancer cells [3].
  • These findings also suggest that the full inhibitory effect of E2 on T synthesis results from a pubertal maturation process, possibly induced by endogenous gonadotropins, which cannot be induced by two weeks of hCG stimulation in prepubertal boys or those with hypogonadotropic hypogonadism [4].

Psychiatry related information on estradiol

  • Central infusions of PRL or placental lactogens (PLs) together with systemic treatment of progesterone (P) and estradiol (E2) stimulate maternal behavior in 1-2 days [5].
  • The data indicate a preferential induction of zr-proteins compared with vitellogenin, both with regard to E2 sensitivity and response time to E2 treatment [6].

High impact information on estradiol


Chemical compound and disease context of estradiol

  • It has been suggested that transforming growth factor-alpha (TGF-alpha) is a mitogenic autocrine growth factor for human breast cancer cells, responsible for mediating the mitogenic effects of 17 beta-estradiol (E2) in responsive cells [3].
  • The responses of serum testosterone (T), 17 alpha-hydroxyprogesterone, and 17 beta-estradiol (E2) to four im injections of hCG (5000 IU/1.7 m2) given on days 0, 4, 7, and 10 were studied in 10 prepubertal and 10 pubertal boys with hypogonadotropic hypogonadism (groups O and P, respectively) [4].
  • These results suggest that the ovaries of postmenopausal women with endometrial cancer secrete significantly more T and A than do the ovaries of women without cancer, while secreting only minimal amounts of E2 and E1 [10].
  • Our data show that the lack of E2 and presence of androgens contribute to progressive renal disease induced by RW hypertension, suggesting that gonadal steroid status is an independent factor in the greater susceptibility men exhibit toward hypertension-associated renal disease compared with women [11].
  • A significant decrease in pulmonary and hepatic edema formation as well as neutrophil infiltration in the lung was observed after E2, flutamide and E2 + flutamide administration [12].

Biological context of estradiol

  • However, both of the transfected clones that constitutively secrete elevated levels of TGF-alpha (A8 and H8) respond to E2 stimulation in vitro by increasing the rate of cellular proliferation and inducing PGR synthesis [3].
  • Histomorphometric analyses of the cross-sections of the tibia revealed that TZP-4238 increased but E2 reduced the periosteal bone formation rate compared with OVX rats [13].
  • While TGF-alpha expression may be essential, it is not sufficient alone to induce the fully E2-independent phenotype [3].
  • In E2-treated rats, which exhibited a LH surge similar in timing to the PRO surge, POMC mRNA levels exhibited a diurnal rhythm strikingly similar to that observed in PRO animals [14].
  • This was followed by normal functional expression of follicular growth and maturation, as reflected by an increase in E2 and i-INH levels, timely ovulation, and normal luteal function [15].

Anatomical context of estradiol

  • According to ISH data, E2 and to a lesser extent B stimulated H19 transcription in the uterus, whereas P inhibited it [16].
  • In agreement with the changes in the BMD of different regions of the femur, TZP-4238 but not E2 increased the physical strength of the femoral diaphysis assessed by a three-point bending test [13].
  • After optimal induction of tissue factor expression by E2 plus MPA, removal of these steroids reduced levels of stromal cell tissue factor mRNA and protein, with virtually complete reversal by day 7 of withdrawal [17].
  • Stromelysin-1 expression by cultured decidual cells isolated from first trimester endometrium was also reduced by MPA and synergistically reduced by E2 plus MPA [18].
  • IGF-I mRNA is barely detected in control myometrium, is significantly increased by E2 treatment, and is augmented even more by the combination of E2 and P4 treatment, whereas little change is noted in myometrial IGF-II or IGF-I receptor mRNA levels [19].

Associations of estradiol with other chemical compounds

  • Both the early transient and late sustained increases in intracellular Ca2+ and PKC translocation were blunted, and the effects of 0.2 nM E2 and 3.2 nM P were specifically antagonized by the receptor blockers ICI 182,780 (200 nM) and RU486 (15 nM), respectively [2].
  • Hyperreactive responses to the combination of 5-HT and U46619 in untreated VMC were significantly and dose-dependently reduced by treatment in vitro with physiological levels of either E2 or P for at least 24 h [2].
  • Both E2 and T specifically stimulated GTHII beta gene expression in cultured juvenile rainbow trout pituitary cells [20].
  • Treatment with E2 or DHT also completely prevented the increase in pro-GnRH mRNA levels induced by ovariectomy [21].
  • Similarly, treatment during the early luteal phase produced a decline in E2 concentrations from 286 +/- 29 to 70 +/- 7 pmol/L and a decline in progesterone concentrations from 20 +/- 1.6 to 1.9 +/- 0.3 nmol/L within 24 h after the last injection [22].

Gene context of estradiol

  • Neutral E2 analogues were found to complement ER alpha(E353A) with similar potencies but with generally lower selectivities [23].
  • The serum levels of E2 (P less than 0.04) as well as those of A, SHBG, and LH (P less than 0.002) were lower in the obese group [24].
  • Uterine smooth muscle IGFBP-3 mRNA levels are negatively regulated, whereas IGFBP-4 and -5 mRNA levels are positively regulated by E2: none of these myometrial IGFBPs appears sensitive to the effects of P4 [25].
  • IGFBP-4 and 5 mRNAs were readily detectable in control myometrium and significantly increased by E2 treatment [25].
  • Both IGF-I and IGFBP-2 are dependent on E2 for significant myometrial expression, and both are further augmented by the addition of P4 to E2 treatment [25].

Analytical, diagnostic and therapeutic context of estradiol

  • Administration of E2 or DHT to castrated animals completely prevented the post castration rise in pro-GnRH mRNA levels [21].
  • To evaluate the time dependency of estrogen action, studies were conducted at baseline and after 1 and 5 weeks of oral administration of ethinyl estradiol (EE; 100 ng/ [26].
  • Ovariectomized rhesus monkeys were treated with placebo, estradiol (E2), or E2 and progesterone (P4) (E2 and P4) for 2 weeks, after which their uteri were removed and cut into thin serial sections for analysis by in situ hybridization [25].
  • On day 12 of pulsatile GnRH administration, plasma E2 levels increased, and LH and FSH pulses followed each GnRH pulse during the frequent sampling study [27].
  • To clarify the nature of these LH responses, we examined, using a 5-min blood-sampling regimen, the afternoon pulsatile pattern of LH release after treatment with appropriate doses of E2 [28].


  1. Direct and sex-specific stimulation by sex steroids of creatine kinase activity and DNA synthesis in rat bone. Sömjen, D., Weisman, Y., Harell, A., Berger, E., Kaye, A.M. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  2. In vitro modulation of primate coronary vascular muscle cell reactivity by ovarian steroid hormones. Minshall, R.D., Miyagawa, K., Chadwick, C.C., Novy, M.J., Hermsmeyer, K. FASEB J. (1998) [Pubmed]
  3. The effects of a constitutive expression of transforming growth factor-alpha on the growth of MCF-7 human breast cancer cells in vitro and in vivo. Clarke, R., Brünner, N., Katz, D., Glanz, P., Dickson, R.B., Lippman, M.E., Kern, F.G. Mol. Endocrinol. (1989) [Pubmed]
  4. Single versus repeated dose human chorionic gonadotropin stimulation in the differential diagnosis of hypogonadotropic hypogonadism. Dunkel, L., Perheentupa, J., Sorva, R. J. Clin. Endocrinol. Metab. (1985) [Pubmed]
  5. Central lactogenic regulation of maternal behavior in rats: steroid dependence, hormone specificity, and behavioral potencies of rat prolactin and rat placental lactogen I. Bridges, R.S., Robertson, M.C., Shiu, R.P., Sturgis, J.D., Henriquez, B.M., Mann, P.E. Endocrinology (1997) [Pubmed]
  6. Oogenesis in Atlantic salmon (Salmo salar L.) occurs by zonagenesis preceding vitellogenesis in vivo and in vitro. Celius, T., Walther, B.T. J. Endocrinol. (1998) [Pubmed]
  7. Identification of target genes in breast cancer cells directly regulated by the SRC-3/AIB1 coactivator. Labhart, P., Karmakar, S., Salicru, E.M., Egan, B.S., Alexiadis, V., O'Malley, B.W., Smith, C.L. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  8. Cannabinoid ligand-receptor signaling in the mouse uterus. Das, S.K., Paria, B.C., Chakraborty, I., Dey, S.K. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  9. Ligand-dependent, transcriptionally productive association of the amino- and carboxyl-terminal regions of a steroid hormone nuclear receptor. Kraus, W.L., McInerney, E.M., Katzenellenbogen, B.S. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  10. Ovarian steroid secretion in postmenopausal women with and without endometrial cancer. Nagamani, M., Hannigan, E.V., Dillard, E.A., Van Dinh, T. J. Clin. Endocrinol. Metab. (1986) [Pubmed]
  11. Gonadal steroid regulation of renal injury in renal wrap hypertension. Ji, H., Menini, S., Mok, K., Zheng, W., Pesce, C., Kim, J., Mulroney, S., Sandberg, K. Am. J. Physiol. Renal Physiol. (2005) [Pubmed]
  12. Effects of 17{beta}-estradiol and flutamide on inflammatory response and distant organ damage following trauma-hemorrhage in metestrus females. Hildebrand, F., Hubbard, W.J., Choudhry, M.A., Thobe, B.M., Pape, H.C., Chaudry, I.H. J. Leukoc. Biol. (2006) [Pubmed]
  13. A new synthetic steroid, osaterone acetate (TZP-4238), increases cortical bone mass and strength by enhancing bone formation in ovariectomized rats. Fuse, H., Fukumoto, S., Sone, H., Miyata, Y., Saito, T., Nakayama, K., Takahashi, H., Matsumoto, T., Ogata, E. J. Bone Miner. Res. (1997) [Pubmed]
  14. Diurnal pattern of proopiomelanocortin gene expression in the arcuate nucleus of proestrous, ovariectomized, and steroid-treated rats: a possible role in cyclic luteinizing hormone secretion. Wise, P.M., Scarbrough, K., Weiland, N.G., Larson, G.H. Mol. Endocrinol. (1990) [Pubmed]
  15. Follicular arrest during the midfollicular phase of the menstrual cycle: a gonadotropin-releasing hormone antagonist imposed follicular-follicular transition. Kettel, L.M., Roseff, S.J., Chiu, T.C., Bangah, M.L., Vale, W., Rivier, J., Burger, H.G., Yen, S.S. J. Clin. Endocrinol. Metab. (1991) [Pubmed]
  16. Steroid hormones modulate H19 gene expression in both mammary gland and uterus. Adriaenssens, E., Lottin, S., Dugimont, T., Fauquette, W., Coll, J., Dupouy, J.P., Boilly, B., Curgy, J.J. Oncogene (1999) [Pubmed]
  17. Steroid-modulated stromal cell tissue factor expression: a model for the regulation of endometrial hemostasis and menstruation. Lockwood, C.J., Nemerson, Y., Krikun, G., Hausknecht, V., Markiewicz, L., Alvarez, M., Guller, S., Schatz, F. J. Clin. Endocrinol. Metab. (1993) [Pubmed]
  18. Ovarian steroid-modulated stromelysin-1 expression in human endometrial stromal and decidual cells. Schatz, F., Papp, C., Toth-Pal, E., Lockwood, C.J. J. Clin. Endocrinol. Metab. (1994) [Pubmed]
  19. Sex steroid regulation of insulin-like growth factor system gene expression and proliferation in primate myometrium. Adesanya, O.O., Zhou, J., Bondy, C.A. J. Clin. Endocrinol. Metab. (1996) [Pubmed]
  20. Differential recruitment of steroid hormone response elements may dictate the expression of the pituitary gonadotropin II beta subunit gene during salmon maturation. Xiong, F., Liu, D., Le Drean, Y., Elsholtz, H.P., Hew, C.L. Mol. Endocrinol. (1994) [Pubmed]
  21. Regulation of pro-gonadotropin-releasing hormone gene expression by sex steroids in the brain of male and female rats. Toranzo, D., Dupont, E., Simard, J., Labrie, C., Couet, J., Labrie, F., Pelletier, G. Mol. Endocrinol. (1989) [Pubmed]
  22. Variable ovarian response to gonadotropin-releasing hormone antagonist-induced gonadotropin deprivation during different phases of the menstrual cycle. Fluker, M.R., Marshall, L.A., Monroe, S.E., Jaffe, R.B. J. Clin. Endocrinol. Metab. (1991) [Pubmed]
  23. Functionally orthogonal ligand-receptor pairs for the selective regulation of gene expression generated by manipulation of charged residues at the ligand-receptor interface of ER alpha and ER beta. Shi, Y., Koh, J.T. J. Am. Chem. Soc. (2002) [Pubmed]
  24. Sex steroid, gonadotropin, cortisol, and prolactin levels in healthy, massively obese women: correlation with abdominal fat cell size and effect of weight reduction. Grenman, S., Rönnemaa, T., Irjala, K., Kaihola, H.L., Grönroos, M. J. Clin. Endocrinol. Metab. (1986) [Pubmed]
  25. Cellular localization and sex steroid regulation of insulin-like growth factor binding protein messenger ribonucleic acids in the primate myometrium. Adesanya, O.O., Zhou, J., Bondy, C.A. J. Clin. Endocrinol. Metab. (1996) [Pubmed]
  26. Estrogenic modulation of the gonadotropin-releasing hormone-stimulated secretory activity of the gonadotrope and lactotrope in prepubertal females with Turner's syndrome. Mauras, N., Rogol, A.D., Veldhuis, J.D. J. Clin. Endocrinol. Metab. (1991) [Pubmed]
  27. Even after priming with ovarian steroids or pulsatile gonadotropin-releasing hormone administration, naltrexone is unable to induce ovulation in women with functional hypothalamic amenorrhea. Couzinet, B., Young, J., Brailly, S., Chanson, P., Schaison, G. J. Clin. Endocrinol. Metab. (1995) [Pubmed]
  28. The development of afternoon minisurges of luteinizing hormone secretion in prepubertal female rats is ovary dependent. Urbanski, H.F., Ojeda, S.R. Endocrinology (1986) [Pubmed]
WikiGenes - Universities