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Introduction The results of the Million Women Study ( Anderson et al. 2003 , Beral et al. 2005 ) have raised concern regarding safety of estrogen or estrogen plus progesterone hormone replacement therapies (HRT). Therefore
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available about their effects on brain functions. Here, we discuss some data concerning their neural effects in animal models and in women having combined oral contraceptive (COC) or hormone replacement therapy (HRT). Observations in animal models
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, astrocytes, hormones, growth factors, etc. are in the arena of the ‘battle between destruction and repair’ in MS ( McQualter & Bernard 2007 , Rodriguez 2007 ). Cell therapy to repair lesions in MS: in search of a rationale Autologous hematopoietic cell
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. Dionne IJ , Kinaman KA & Poehlman ET 2000 Sarcopenia and muscle function during menopause and hormone-replacement therapy. Journal of Nutrition, Health and Aging 4 156 –161. Glass DJ 2005 Skeletal muscle hypertrophy
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Intranasal administration of hormone replacement therapy presents an original plasma kinetic profile with transient estrogen levels giving rise to the concept of pulsed therapy. To further understand the molecular effects of this new therapy, we have compared the effects of pulsed and continuous estradiol treatments on two critical aspects of estradiol action: gene expression and cell proliferation. Cells were stimulated with estradiol as 1-h pulsed or 24-h continuous treatments at concentrations such that the 24-h exposure (concentration x time) was identical in both conditions. In MCF7 cells, the transcriptional activity of estrogen receptors (ER) on a transiently transfected responsive estrogen response element-luciferase reporter construct was shown to be drastically (approximately 10-fold) and similarly stimulated after both treatments. Moreover, the increased mRNA expression of three representative estradiol-sensitive genes (pS2, cathepsin D, progesterone receptor), evaluated by Northern blot, was identical after 1-h pulse with 7 nM estradiol or continuous treatment with 0.29 nM estradiol with the same kinetic profile over 48 h. Proliferation was quantified by a histomorphometric method on primary cultures of human normal breast cells from reduction mammoplasties and using a fluorescence DNA assay in six human breast cancer cell lines which were ER positive or negative. After a 7-day treatment period, estradiol had no effect on the proliferation of the three ER negative cell lines (BT20, MDA MB231, SK BR3) but significantly stimulated the proliferation of the normal cells and of the three tumoral hormone-sensitive cell lines (MCF7, T47D, ZR 75-1); both hormone treatments producing the same increases in cell growth. In conclusion, we have shown that the genomic or proliferative effects of estradiol were identical with pulsed or continuous treatments, thus indicating that estrogenic effects are not strictly related to concentrations but rather to total hormone exposure.
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action of testosterone action via the AR in bone to influence fat deposition by generating a unique mouse model, PC-AR Gene Replacements. This mouse model replaces the AR gene only in pluripotent bone marrow mesenchymal progenitor cells (BM-PCs) of male
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hormone-replacement therapy in the Million Women Study . Lancet 362 419 – 427 . ( https://doi.org/10.1016/s0140-6736(0314065-2 ) Beral V Reeves G Bull D Green J Million Women Study Collaborators 2011 Breast cancer risk in relation to the
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Lung volumes and respiratory muscle strength in adult patients with childhood- or adult-onset growth hormone deficiency: effect of 12 months’ growth hormone replacement therapy . European Journal of Endocrinology 135 553 – 558 . ( doi:10.1530/eje.0
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uterine bleeding and endometrial and breast cancers. Along the way, the use of synthetic progestins has led to controversy, most particularly its inclusion in hormone-replacement therapy (HRT) to prevent the potentially malignant effects of unopposed
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), the Heart and Estrogen/Progestin Replacement Study (HERS) I, HERS II ( Hulley et al. 2002 ) and the Estonian postmenopausal hormone therapy clinical trial ( Veerus et al. 2006 ) among others ( Nachtigall et al. 1979 , Herrington et al. 2000
