Efecto farmacológico de inhibidores de calmodulina sobre los niveles de RNAm de prolactina incrementados por el 17 b-estradiol [por] Rosa Patricia Hernández Torres

Tesis (Maestría en Ciencias con Especialidad en Biología Molecular e Ingeniería Genética) U.A.N.L.

Comparison of the global gene expression profiles produced by methylparaben, n-butylparaben and 17 beta-oestradiol in MCF7 human breast cancer cells

Since the alkyl esters of p-hydroxybenzoic acid (parabens) can be measured intact in the human breast and possess oestrogenic properties, it has been suggested that they could contribute to an aberrant burden of oestrogen signalling in the human breast and so play a role in the rising incidence of breast cancer. However, although parabens have been shown to regulate a few single genes (reporter genes, pS2, progesterone receptor) in a manner similar to that of 17 beta-oestradiol, the question remains as to the full extent of the similarity in the overall gene profile induced in response to parabens compared with 17 beta-oestradiol. The GE-Amersham CodeLink 20 K human expression microarray system was used to profile the expression of 19881 genes in MCF7 human breast cancer cells following a 7-day exposure to 5 x 10(-4) m methylparaben, 10(-5) m n-butylparaben and 10(-8) m 17 beta-oestradiol. At these concentrations, the parabens gave growth responses in MCF7 cells of similar magnitude to 17 beta-oestradiol. The study identified genes which are upregulated or downregulated to a similar extent by methylparaben, n-butylparaben and 17 beta-oestradiol. However, the majority of genes were not regulated in the same way by all three treatments. Some genes responded differently to parabens from 17 beta-oestradiol, and furthermore, differences in expression of some genes could be detected even between the two individual parabens. Therefore, although parabens possess oestrogenic properties, their mimicry in terms of global gene expression patterns is not perfect and differences in gene expression profiles could result in consequences to the cells that are not identical to those following exposure to 17 beta-oestradiol. Copyright (c) 2006 John Wiley & Sons, Ltd.

Concentrações séricas de progesterona, 17 b-estradiol e cortisol durante o final do próestro, estro e diestro gestacional em cadelas

Neste estudo, foram utilizadas 7 cadelas sem raça definida, adultas e hígidas, copuladas com macho hígido, após exame andrológico, para acompanhamento das variações hormonais de progesterona, 17b-estradiol e cortisol a partir do final do próestro, durante o estro e diestro gestacional em fêmeas da espécie canina. As avaliações séricas do cortisol foram iniciadas no período de estro. A citologia vaginal esfoliativa foi utilizada como parâmetro auxiliar para a determinação das fases do ciclo estral, mais especificamente para análise do melhor momento para cópula, através da presença das células superficiais queratinizadas visibilizadas nas lâminas. Os resultados obtidos mostraram concentrações médias de progesterona elevando-se discretamente no final do próestro (de 1,56 para 2,85ng ml-1), concomitante com o início do declínio dos valores de estradiol no mesmo período (de 20,93 para 18,81pg ml-1). Durante a gestação pôde-se observar concentrações elevadas de progesterona (36,90ng ml-1), havendo declínio apenas no terço final (4,10ng ml-1), quando também pôde ser notada, por um momento, ligeira elevação das concentrações médias de 17b-estradiol (2,46pg ml-1). O aumento do cortisol sérico foi notado na última semana da gestação havendo, antes disso, alterações significativas (P<0,05) nas concentrações séricas baseadas nos padrões descritos em literatura. No pós-parto imediato a redução do cortisol sérico (6,52ng ml-1) foi considerada relevante de acordo com as concentrações detectadas na última semana da gestação (22,27ng ml-1). A progesterona esteve mantida em níveis basais no pós-parto imediato (< 1ng ml-1).

Effect of progesterone and/or estradiol treatments prior to induction of ovulation on subsequent luteal lifespan in anestrous Nelore cows

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Osteocalcin immunolabeling during the alveolar healing process in ovariectomized rats treated with estrogen or raloxifene

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Histomorphometric analysis and immunolocalization of RANKL and OPG during the alveolar healing process in female ovariectomized rats treated with oestrogen or raloxifene

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Hormonal therapy in the senescence: Prostatic microenvironment structure and adhesion molecules

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Changes in luteinizing hormone secretion after estradiol treatment in prepubertal Nelore heifers

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efeitos iniciais da ovariectomia e do tratamento com estrógeno e isoflavonas da soja, isolados e associados, na reparação óssea alveolar e no útero de ratas

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influência dos níveis plasmáticos de estrógeno na resposta ao tratamento periodontal relacionado à causa em mulheres na fase de menopausa

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Differential expression of aromatase, estrogen receptor alpha and 17 beta-HSD associated with the processes of total testicular regression and recrudescence in the bat Myotis nigricans (Chiroptera: Vespertilionidae)

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Estradiol stimulates tyrosine phosphorylation of the insulin-like growth factor-1 receptor and insulin receptor substrate-1 in the uterus.

The signaling pathways associated with estrogen-induced proliferation of epithelial cells in the reproductive tract have not been defined. To identify receptor tyrosine kinases that are activated in vivo by 17 beta-estradiol (E2), uteri from ovariectomized mice were examined for enhanced tyrosine phosphorylation of various receptors and a receptor substrate following treatment with this hormone. Within 4 hr after hormone exposure, extracts showed increased phosphotyrosine (P-Tyr) immunoreactivity at several bands, including 170- and 180-kDa; these bands were still apparent at 24 hr after E2. Analysis of immunoprecipitates from uterine extracts revealed that E2 enhanced tyrosine phosphorylation of the insulin-like growth factor-1 receptor (IGF-1R) and insulin receptor substrate-1 (IRS-1) by 6 hr. Comparison of supernatants from IRS-1 and control rabbit IgG immunoprecipitates indicated that the 170-kDa P-Tyr band in extracts was equivalent to IRS-1. The receptors for epidermal growth factor, platelet-derived growth factor, and basic fibroblast growth factor did not exhibit an E2-induced increase in P-Tyr content. The nonestrogenic steroid hormones examined did not stimulate the P-Tyr content of IGF-1R or IRS-1. Immunolocalization of P-Tyr and IRS-1 revealed strong reactivity in the epithelial layer of the uterus from E2-treated mice, suggesting that the majority of P-Tyr bands observed in immunoblots originate in the epithelium. Since hormonal activation of IRS-1 is epithelial, estrogen-specific, and initiated before maximal DNA synthesis occurs following treatment with hormone, this protein, as part of the IGF-1R pathway, may be important in mediating estrogen-stimulated proliferation in the uterus.

Estrogen reduces atherosclerotic lesion development in apolipoprotein E-deficient mice.

We have studied the effects of endogenous and exogenous estrogen on atherosclerotic lesions in apolipoprotein E-deficient mice. Female mice ovariectomized (OVX) at weaning displayed increases (P < 0.01) in fatty streak lesions in the proximal aorta and aortic sinus compared with female mice with intact ovarian function. These differences between the OVX and sham controls were apparent in both chow- and "Western-type" diet-fed mice. Moreover, increases in lesion size following OVX occurred without changes in plasma cholesterol. Hormone replacement with subdermal 17-beta-estradiol pellets releasing either 6, 14, or 28 micrograms/day significantly decreased (P < 0.001) atherosclerotic lesion area in both male and OVX female mice. In contrast, neither 17-alpha-estradiol (28 micrograms/day) or tamoxifen (85 micrograms/day) affected lesion progression in OVX female mice. In the Western diet-fed group, exogenous estradiol markedly reduced plasma cholesterol and triglycerides, whereas, in animals fed the chow diet, exogenous estrogen and tamoxifen treatment only decreased plasma and very low density lipoprotein triglycerides. However, lesion area was only weakly correlated with plasma cholesterol and triglycerides, 0.35 and 0.44 tau values, respectively (P < 0.01). In summary, in the apolipoprotein E-deficient mouse 17-beta-estradiol protects against atherosclerotic lesion formation, and this can only be partially explained through effects on plasma lipoprotein levels.