Estrogen

Summary

Estrogen or oestrogen (see spelling differences) is a category of sex hormone responsible for the development and regulation of the female reproductive system and secondary sex characteristics. There are three major endogenous estrogens that have estrogenic hormonal activity: estrone (E1), estradiol (E2), and estriol (E3). Estradiol, an estrane, is the most potent and prevalent. Another estrogen called estetrol (E4) is produced only during pregnancy. Estrogens are synthesized in all vertebrates and some insects. Quantitatively, estrogens circulate at lower levels than androgens in both men and women. While estrogen levels are significantly lower in males than in females, estrogens nevertheless have important physiological roles in males. Like all steroid hormones, estrogens readily diffuse across the cell membrane. Once inside the cell, they bind to and activate estrogen receptors (ERs) which in turn modulate the expression of many genes. Add

Official source

https://en.wikipedia.org/wiki/Estrogen

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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

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

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