Œstrogène

Résumé

vignette|Graphiques d'œstrogènes Les œstrogènes ou estrogènes (prononcé : , ou pour la première graphie) constituent un groupe de stéroïdes, dont la fonction, à l'état naturel, est d'être une hormone sexuelle femelle primaire. Ils sont produits en premier lieu par le développement des follicules des ovaires et par le placenta. Certains œstrogènes sont également produits en petites quantités par d'autres tissus tels le foie, la surrénale, les seins et le tissu adipeux. Ces sources secondaires d'œstrogènes sont particulièrement importantes chez les femmes lors de la post-ménopause. Les trois œstrogènes naturels sont l'estradiol, l'estriol et l'estrone. Dans le corps, ils sont tous produits au départ d'androgènes sous l'effet d'enzymes. L'estradiol est produit à partir de la testostérone et l'estrone à partir de l'androstènedione. L'estrone est beaucoup moins puissante que l'estradiol, et chez les femmes en post-ménopause, on trouve plus d'estrone que d'estradiol. Les œstrogènes jouen

Source officielle

https://fr.wikipedia.org/wiki/%C5%92strog%C3%A8ne

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Lestradiol ou œstradiol (à ne pas confondre avec l'œstriol ou estriol qui est un autre œstrogène) est un dérivé naturel du métabolisme du cholestérol (via la testostérone) qui est nécessaire au main

La testostérone est une hormone stéroïdienne, du groupe des androgènes. Chez les mammifères, la testostérone est sécrétée essentiellement par les gonades, c'est-à-dire les testicules des mâles et le

La ménopause, du grec méno, règles, et pause, arrêt, appelée aussi âge climatérique, est l'arrêt du cycle ovarien, le symptôme le plus visible étant l'arrêt définitif des règles. Ce phénomène biologi

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Histamine is a ubiquitous brain neurotransmitter. Estrogen hormones have been shown to increase histamine effects on neurons located in the ventromedial nucleus of the hypothalamus (VMN) (Kow et al, 2005a). This study has been set up to find candidate pathways to explain the mechanism(s) by which estradiol does this enhancement. Therefore, we decided to look at which histamine receptors are involved in histamine-induced depolarization. Previous studies (Zhou et al, 2007) showed that in mice only the histamine receptor H1 (H1-R) is involved in histamine actions on VMN neurons. It seems however that in rats the mechanism includes more than one receptor. By using histamine agonists (betahistidine and dimaprit) in whole cell patch clamp experiments we revealed that both H1-R and histamine receptor H2 (H2-R) coexist and can mediate opposite actions of histamine on individual VMN neurons. To refine our pharmacological study histamine antagonists were used too. The blocking of both these two receptors revealed that a histamine response is the sum of the depolarization and hyperpolarization by H1-R and H2-R, respectively. Colocalization of H1-R and H2-R on the same cells was therefore suggested and will be evaluated by Immunohistochemistry.

2008

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Estrogen receptor signaling in the human breast epithelium

Céline Berthe Constantin

Breast cancer is the most diagnosed malignancy in women worldwide, making effective prevention strategies crucial. Hormonal contraceptives, consisting of a synthetic progesterone receptor agonist alone or in combination with an estrogen, are used by millions of women worldwide and have been linked to increased breast cancer risk. To date, their mechanisms of action on human breast epithelial cells (HBECs) remain elusive. We have previously shown that the mouse intraductal model in which HBECs are grafted to the milk ducts of immunocompromised mice preserves hormone receptor expression. We exploited this model to assess if 17alpha-ethinyl estradiol (EE2), the predominant estrogenic component of combined oral contraceptives (OCs), has a distinct activity profile from that of the natural estrogen 17beta-estradiol (E2) in HBECs and characterized methods for stable and long-term estrogen delivery.We show that both E2 and EE2 increased the in vivo growth of HBECS, with the former estrogen being slightly more potent. E2 and EE2-treated glands showed similar proliferation indices 21 days after treatment and displayed similar transcriptomic profiles with robust gene signatures. Our data suggest that the increased risk of breast cancer associated with the use of OCs is not attributed to EE2, but rather to the progestin used in combination. We recently showed that progestins with androgenic properties promote HBEC proliferation but progestins with anti-androgenic properties do not.

EPFL2022

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Differential Roles of MAPK Kinases MKK3 and MKK6 in Osteoclastogenesis and Bone Loss

Mario Michael Zaiss

Bone mass is maintained by osteoclasts that resorb bone and osteoblasts that promote matrix deposition and mineralization. Bone homeostasis is altered in chronic inflammation as well as in post-menopausal loss of estrogen, which favors osteoclast activity that leads to osteoporosis. The MAPK p38 alpha is a key regulator of bone loss and p38 inhibitors preserve bone mass by inhibiting osteoclastogenesis. p38 function is regulated by two upstream MAPK kinases, namely MKK3 and MKK6. The goal of this study was to assess the effect of MKK3- or MKK6-deficiency on osteoclastogenesis in vitro and on bone loss in ovariectomy-induced osteoporosis in mice. We demonstrated that MKK3 but not MKK6, regulates osteoclast differentiation from bone marrow cells in vitro. Expression of NFATc1, a master transcription factor in osteoclastogenesis, is decreased in cells lacking MKK3 but not MKK6. Expression of osteoclast-specific genes Cathepsin K, osteoclast-associated receptor and MMP9, was inhibited in MKK3-/- cells. The effect of MKK-deficiency on ovariectomy-induced bone loss was then evaluated in female WT, MKK3-/- and MKK6-/- mice by micro-CT analysis. Bone loss was partially inhibited in MKK3-/- as well as MKK6-/- mice, despite normal osteoclastogenesis in MKK6-/- cells. This correlated with the lower osteoclast numbers in the MKK-deficient ovariectomized mice. These studies suggest that MKK3 and MKK6 differentially regulate bone loss due to estrogen withdrawal. MKK3 directly mediates osteoclastogenesis while MKK6 likely contributes to pro-inflammatory cytokine production that promotes osteoclast formation.

Public Library of Science2014

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