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

AC1NWAOC     [(6S,10R,13S,17R)-17- ethanoyl-6,10,13...

Synonyms: BSPBio_001953, KBioGR_000477, KBioSS_001375, CCG-38954, SureCN13941346, ...
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 Medroxyprogesterone acetate


Psychiatry related information on Medroxyprogesterone acetate

  • RESULTS: MPA exposure 4 or 6 weeks after DMBA reduced the latency period for appearance of tumors in a dose-dependent manner and increased tumor incidence [6].
  • CEE + MPA did not significantly influence positive affect, negative affect, or depressive symptoms [7].
  • The time study of the effect of E showed that enhancement of AA required at least 10 h of incubation of E with MPA conditioned cells [8].
  • Heart rate variability (HRV) was calculated in time and frequency domains during various sleep stages on and off MPA, and the results were correlated to respiratory variables [9].
  • Forty men, ages 16 to 78 years, with sex-offending behavior, were treated with combined medroxyprogesterone acetate (MPA), group therapy, and individual psychotherapy [10].

High impact information on Medroxyprogesterone acetate


Chemical compound and disease context of Medroxyprogesterone acetate

  • RU-486 also delayed the latency period but failed to reduce overall tumor incidence when animals were exposed to MPA at 6 weeks after DMBA treatment, indicating that other factors may also control MPA-induced acceleration [6].
  • This study evaluated the effectiveness of parenteral medroxyprogesterone acetate (MPA) in reducing the frequency and severity of these hot flashes [1].
  • Since one of the possible explanations for this effect was its progestagenic effects, we decided to investigate whether progesterone (Pg) alone could also induce mammary adenocarcinomas in our model and if MPA at doses lower than those used to establish the model was also carcinogenic [14].
  • Oestrogen receptor (ER) and progesterone receptor (PR) content and the response in vitro to tamoxifen (T), medroxyprogesterone acetate (MPA) and to a combination of the two hormones were determined in 21 epithelial ovarian carcinomas [15].
  • CONCLUSION: Treatment with LA depot plus conjugated equine Es and MPA for 2 years was a safe and effective therapy for women with endometriosis and pelvic pain in this small retrospective study [16].

Biological context of Medroxyprogesterone acetate

  • To study RU 486 involvement in steroid withdrawal leading to menstruation, HESCs were decidualized during 10 days incubation with E2 + MPA, and parallel cultures were kept in E2 + MPA or withdrawn to either control or RU 486-containing medium [17].
  • MPA stimulated cell growth and PRL production rate during days 5-20 of culture [18].
  • This combination of CEE and MPA resulted in a 60% improvement (P less than 0.05) compared to the luteal phase of control months in both behavioral (14.1 +/- 3.9 vs. 4.2 +/- 0.8) and total (17.8 +/- 4.8 vs. 6.5 +/- 1.8) symptoms [19].
  • However, it appears that MPA with significant glucocorticoid (GC) activity may decrease bone density [20].
  • Medroxyprogesterone acetate (MPA) and the anti-progestin RU 38.486, which possess glucocorticoid and antiglucocorticoid activity, respectively, cause receptor down-regulation at lower concentrations than their Kdi for [3H] ORG 2058 binding sites [21].

Anatomical context of Medroxyprogesterone acetate

  • PRL was one of the five major secretory proteins (23-25K, 32K, 42K, 78K, and 150K daltons, sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing condition) induced by MPA and RLX in endometrial stromal cells [18].
  • To study the interaction of P(4) and F on the regulation of PGDH, we treated chorion and placental trophoblast cells in culture with combinations of F, dexamethasone, P(4), trilostane, and medroxyprogesterone acetate (MPA) [22].
  • A representative analogue, 8, demonstrated similar oral potency to MPA in the uterine wet weight/mammary gland morphology assay in ovariectomized rats [23].
  • Serum progesterone concentrations remained low, and corpora lutea regressed, although viable fetuses were maintained with MPA [24].
  • MPA down-regulated PgR content and increased uterus weight (36%), but failed to modify ER and PgR nuclear retention [25].

Associations of Medroxyprogesterone acetate with other chemical compounds

  • Progesterone was 20-40% less effective in stimulating PRL than MPA [18].
  • Immunoblot analysis using a specific polyclonal antibody against stromelysin-1 revealed that the progestin medroxyprogesterone acetate (MPA) produced a time-dependent reduction in a band at 50,000 mol wt [26].
  • E2, MPA, E2 plus MPA, and GnRH analog treatments resulted in an increase in total TGF beta 1 production, whereas GnRH agonist and GnRH-Ant2, but not GnRH-An1, inhibited active TGF beta 1 (P < 0.05) [27].
  • In a primate model for long-term HRT, surgically, postmenopausal cynomolgus macaques were treated for 35 months with conjugated equine estrogens (CEE), medroxyprogesterone acetate (MPA), CEE + MPA and tamoxifen (n = 5 in all groups) [28].
  • We examined the effects of two clinically used progestogens, progesterone and medroxyprogesterone acetate (MPA), on prostacyclin production by cultured human umbilical vein endothelial cells (HUVEC) and the possible role of progesterone receptors and both COX enzymes [29].

Gene context of Medroxyprogesterone acetate

  • The expression of p27 in hyperplastic epithelia before the MPA treatment was negligible, whereas it was greatly increased after the treatment [30].
  • Progesterone and MPA, both at 10 nmol/l, increased mRNA expression and protein content of both COX [29].
  • RESULTS: With MPA, FSH decreased 42.7% (P <.001, 95% confidence interval [CI] -54.2, -31.6), LH 62.1% (P <.01; 95% CI -81. 0, -32.6), and SHBG 58.1% (P <.001; 95% CI -63.0, -43.9) [31].
  • Tam + MPA association produced the same results as Tam alone for ER and PgR nuclear retention, but receptor content was not significantly different from that of controls [25].
  • In stromal cells, MPA alone caused a slight increase (2-4-fold) of the production rate of IGFBP-1 whereas MPA plus RLX synergistically increased (>40-fold) the IGFBP-1 production [32].

Analytical, diagnostic and therapeutic context of Medroxyprogesterone acetate

  • Postmenopausal women received daily doses of conjugated equine estrogen (CEE, 0.625 mg) plus medroxyprogesterone acetate (MPA, 2.5 mg) (standard-dose group, n = 18), CEE (0.3 mg) plus MPA (2.5 mg) (low-dose group, n = 18), or no treatment (control group, n = 15) for 3 months [33].
  • After treatment with CE and medroxyprogesterone acetate (MPA), LH and PRL both increased (P less than 0.05 and P less than 0.01, respectively) [34].
  • Quantitative real-time RT-PCR analysis showed a rapid and strong upregulation of hDlg5 mRNA in cells treated with synthetic progestin medroxyprogesterone acetate (MPA) in the presence of estrogen in MCF-7, T47D and ZR-75-1 cells [35].
  • C(21) Progestin medroxyprogesterone acetate (MPA) is one of the most commonly prescribed progestins for hormone replacement therapy and in gynecologic practice [20].
  • OBJECTIVES: To evaluate the effect of medroxyprogesterone acetate (MPA) therapy on pulmonary arterial pressure (PAP), exhaled nitric oxide (NO), electrocardiogram (ECG), and on arterial blood gases (ABG) [36].


  1. Parenteral medroxyprogesterone for the management of luteinizing hormone releasing hormone induced hot flashes in men with advanced prostate cancer. Langenstroer, P., Kramer, B., Cutting, B., Amling, C., Poultan, T., Lance, R., Thrasher, J.B. J. Urol. (2005) [Pubmed]
  2. Adrenal steroids as parameters of the bioavailability of MA and MPA. Willemse, P.H., Dikkeschei, L.D., Tjabbes, T., van Veelen, H., Sleijfer, D.T. Eur. J. Cancer (1990) [Pubmed]
  3. Medroxyprogesterone-induced endocrine alterations after menopause. Saaresranta, T., Irjala, K., Polo-Kantola, P., Polo, O. Menopause (New York, N.Y.) (2002) [Pubmed]
  4. Estrogen and progestagens differentially modulate vascular proinflammatory factors. Sunday, L., Tran, M.M., Krause, D.N., Duckles, S.P. Am. J. Physiol. Endocrinol. Metab. (2006) [Pubmed]
  5. Efficacy of medroxyprogesterone treatment in infertile women with endometriosis: a prospective, randomized, placebo-controlled study. Harrison, R.F., Barry-Kinsella, C. Fertil. Steril. (2000) [Pubmed]
  6. Natural and synthetic progestins accelerate 7,12-dimethylbenz[a]anthracene-initiated mammary tumors and increase angiogenesis in Sprague-Dawley rats. Benakanakere, I., Besch-Williford, C., Schnell, J., Brandt, S., Ellersieck, M.R., Molinolo, A., Hyder, S.M. Clin. Cancer Res. (2006) [Pubmed]
  7. Effects of combination estrogen plus progestin hormone treatment on cognition and affect. Resnick, S.M., Maki, P.M., Rapp, S.R., Espeland, M.A., Brunner, R., Coker, L.H., Granek, I.A., Hogan, P., Ockene, J.K., Shumaker, S.A. J. Clin. Endocrinol. Metab. (2006) [Pubmed]
  8. Modulation of aromatase activity in human endometrial stromal cells by steroids, tamoxifen and RU 486. Tseng, L., Mazella, J., Sun, B. Endocrinology (1986) [Pubmed]
  9. Medroxyprogesterone improves cardiac autonomic control in postmenopausal women with respiratory insufficiency. Virtanen, I., Polo, O., Saaresranta, T., Kuusela, T., Polo-Kantola, P., Ekholm, E. Respiratory medicine. (2004) [Pubmed]
  10. Depo provera treatment for sex offending behavior: an evaluation of outcome. Meyer, W.J., Cole, C., Emory, E. The Bulletin of the American Academy of Psychiatry and the Law. (1992) [Pubmed]
  11. Regulation of synthesis of the transformation-induced protein, leukocyte plastin, by ovarian steroid hormones. Leavitt, J., Chen, Z.P., Lockwood, C.J., Schatz, F. Cancer Res. (1994) [Pubmed]
  12. Depo-medroxyprogesterone in Women on Antiretroviral Therapy: Effective Contraception and Lack of Clinically Significant Interactions. Cohn, S.E., Park, J.G., Watts, D.H., Stek, A., Hitti, J., Clax, P.A., Yu, S., Lertora, J.J. Clin. Pharmacol. Ther. (2007) [Pubmed]
  13. Mechanism of cortisol/progesterone antagonism in the regulation of 15-hydroxyprostaglandin dehydrogenase activity and messenger ribonucleic acid levels in human chorion and placental trophoblast cells at term. Patel, F.A., Funder, J.W., Challis, J.R. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
  14. Progesterone induction of mammary carcinomas in BALB/c female mice. Correlation between progestin dependence and morphology. Kordon, E.C., Molinolo, A.A., Pasqualini, C.D., Charreau, E.H., Pazos, P., Dran, G., Lanari, C. Breast Cancer Res. Treat. (1993) [Pubmed]
  15. Steroid receptors and response of ovarian cancer to hormones in vitro. Grönroos, M., Kangas, L., Mäenpää, J., Vanharanta, R., Nieminen, A.L., Johansson, R. British journal of obstetrics and gynaecology. (1984) [Pubmed]
  16. Gonadotropin-releasing hormone agonist plus estrogen-progestin "add-back" therapy for endometriosis-related pelvic pain. Friedman, A.J., Hornstein, M.D. Fertil. Steril. (1993) [Pubmed]
  17. Biological mechanisms underlying the clinical effects of RU 486: modulation of cultured endometrial stromal cell stromelysin-1 and prolactin expression. Schatz, F., Papp, C., Aigner, S., Krikun, G., Hausknecht, V., Lockwood, C.J. J. Clin. Endocrinol. Metab. (1997) [Pubmed]
  18. Differential effects of progestin and relaxin on the synthesis and secretion of immunoreactive prolactin in long term culture of human endometrial stromal cells. Zhu, H.H., Huang, J.R., Mazella, J., Rosenberg, M., Tseng, L. J. Clin. Endocrinol. Metab. (1990) [Pubmed]
  19. Successful treatment of severe premenstrual syndrome by combined use of gonadotropin-releasing hormone agonist and estrogen/progestin. Mortola, J.F., Girton, L., Fischer, U. J. Clin. Endocrinol. Metab. (1991) [Pubmed]
  20. Pharmacologic doses of medroxyprogesterone may cause bone loss through glucocorticoid activity: an hypothesis. Ishida, Y., Ishida, Y., Heersche, J.N. Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA. (2002) [Pubmed]
  21. The relationship between affinity of progestins and antiprogestins for the progesterone receptor in breast cancer cells (ZR-PR-LT) and ability to down-regulate the receptor: evidence for heterospecific receptor modulation via the glucocorticoid receptor. van den Berg, H.W., Lynch, M., Martin, J.H. Eur. J. Cancer (1993) [Pubmed]
  22. Cortisol/progesterone antagonism in regulation of 15-hydroxysteroid dehydrogenase activity and mRNA levels in human chorion and placental trophoblast cells at term. Patel, F.A., Challis, J.R. J. Clin. Endocrinol. Metab. (2002) [Pubmed]
  23. 5-Benzylidene 1,2-dihydrochromeno[3,4-f]quinolines, a novel class of nonsteroidal human progesterone receptor agonists. Tegley, C.M., Zhi, L., Marschke, K.B., Gottardis, M.M., Yang, Q., Jones, T.K. J. Med. Chem. (1998) [Pubmed]
  24. Control of corpus luteum function in the pregnant rabbit: role of estrogen and lack of a direct luteotropic role of the placenta. Gadsby, J.E., Keyes, P.L., Bill, C.H. Endocrinology (1983) [Pubmed]
  25. Effects on mouse uterus of three antitumoral drugs acting upon estrogen and progesterone receptors directly and through other transduction pathways. Actis, A.M., Dorfman, V.B., Caruso, S.P., Levin, E. Biochem. Pharmacol. (1998) [Pubmed]
  26. 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]
  27. Gonadotropin-releasing hormone (GnRH) and GnRH receptor gene expression in human myometrium and leiomyomata and the direct action of GnRH analogs on myometrial smooth muscle cells and interaction with ovarian steroids in vitro. Chegini, N., Rong, H., Dou, Q., Kipersztok, S., Williams, R.S. J. Clin. Endocrinol. Metab. (1996) [Pubmed]
  28. Effects of long-term HRT and tamoxifen on the expression of progesterone receptors A and B in breast tissue from surgically postmenopausal cynomolgus macaques. Isaksson, E., Wang, H., Sahlin, L., von Schoultz, B., Cline, J.M., von Schoultz, E. Breast Cancer Res. Treat. (2003) [Pubmed]
  29. Progestogens stimulate prostacyclin production by human endothelial cells. Hermenegildo, C., Oviedo, P.J., García-Martínez, M.C., García-Pérez, M.A., Tarín, J.J., Cano, A. Hum. Reprod. (2005) [Pubmed]
  30. Involvement of cyclin-dependent kinase inhibitor p27Kip1 in growth inhibition of endometrium in the secretory phase and of hyperplastic endometrium treated with progesterone. Shiozawa, T., Nikaido, T., Nakayama, K., Lu, X., Fujii, S. Mol. Hum. Reprod. (1998) [Pubmed]
  31. Prolonged endocrine responses to medroxyprogesterone in postmenopausal women with respiratory insufficiency. Saaresranta, T., Irjala, K., Polo-Kantola, P., Helenius, H., Polo, O. Obstetrics and gynecology. (2000) [Pubmed]
  32. Disparate effects of relaxin and TGFbeta1: relaxin increases, but TGFbeta1 inhibits, the relaxin receptor and the production of IGFBP-1 in human endometrial stromal/decidual cells. Mazella, J., Tang, M., Tseng, L. Hum. Reprod. (2004) [Pubmed]
  33. A comparison of low-dose and standard-dose oral estrogen on forearm endothelial function in early postmenopausal women. Sanada, M., Higashi, Y., Nakagawa, K., Tsuda, M., Kodama, I., Kimura, M., Chayama, K., Ohama, K. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
  34. The effects of estrogen and progestin on endogenous opioid activity in oophorectomized women. Shoupe, D., Montz, F.J., Lobo, R.A. J. Clin. Endocrinol. Metab. (1985) [Pubmed]
  35. HDLG5/KIAA0583, encoding a MAGUK-family protein, is a primary progesterone target gene in breast cancer cells. Purmonen, S., Ahola, T.M., Pennanen, P., Aksenov, N., Zhuang, Y.H., Tuohimaa, P., Ylikomi, T. Int. J. Cancer (2002) [Pubmed]
  36. Effect of medroxyprogesterone on pulmonary arterial pressure, exhaled nitric oxide, ECG and arterial blood gases. Saaresranta, T., Uotila, P., Saraste, M., Irjala, K., Hartiala, J., Polo, O. J. Intern. Med. (2002) [Pubmed]
WikiGenes - Universities