Estrogen synthesis and signaling pathways during …

Estradiol (E2) is a steroid hormone and is part of the oestrogens group of hormones and is the principle oestrogen in females. Estrone and estriol are chemically similar to estradiol but are found in lower concentrations and have a lower estrogenic activity. Production of oestrogens occurs in the ovary via , the and the Zona reticularis of the . In males in it is produced in sertoli cells found in the testes. Estradiol is synthesised from cholestrol.

Oestrogens have a number of functions related to reproduction and other areas of physiology. In relation to the reproductive role of oestrogens, they stimulate follicular growth and maturation, induce the female to begin displaying oestrous behaviour to facilitate mating, prepare the external genitalia for copulation and create favourable conditions for the development of fertilised egg cells. Oestrogens also contribute to the growth and development of mammary tissue and prepare the uterus for parturition.
Effects on reproductive organs:
Vagina: slight mucous secretion, hyperaemia, oedema
Cervix: relaxation, liquification of mucous plug (causing the bull string)
Uterus: stimulates uterine gland development, sensitization of the endometrium to oxytocin, immune activation (local), leucocyte infiltration, secretion of PGF2a and PGE2
Fallopian tube: increased motility and cilia activity
Mammary gland: stimulates mammary duct development
Corpus luteum: Luteolytic (bovine and ovine) but luteotrophic (equine and porcine)

Where oestrogens stimulate growth of follicles in the ovaries, oestrogens secreted from the ovary in the ( and ) lead to hypertrophy of the epithelium and the endometrium. Secretory glands within the uterus enlarge and secretion is initiated leading to thickening of tissues. The blood vessels supplying the uterus and external genitalia dilate and blood flow to these areas increases significantly. Oedema occurs within the uterus and surrounding connective tissues. Oestrogen also causes increased uterine muscle tone. In the cervix oestrogens stimulate increased mucus secretion and the vaginal epithelium becomes keratinised.

In males the target tissue is the brain where it causes maturation of the brain during development. This maturation process ensures the appropriate development of male sexual behaviours. E2 in the male also inhibits long bone growth.

Estrogen synthesis and signaling pathways during ..

20/01/2016 · Blockade of estrogen synthesis in the ..

PPT - Estrogens, Progestins, & Hormone Therapy …

To date, there is no established role for "alternative and complementary medicines"in the treatment of any liver disease, though it's possible some of the herbalremedies might have some effect.

Estrogens, Progestins, & Hormone Therapy

(Future pathologists: there may be parenchymalinvolvement also; zones 1 and 2 are usually sparedbut zone 3 may be inflamed like the portal)The Banff "rejection activity index" gives a score from 0-9, the sum of 0-3 for each of the aboveBILE DUCT STENOSIS can develop late after surgery (scar contracts).

Induces synthesis of progesterone receptors

hCG is a form of glycoprotein that is synthesised within the trophoblast cells of a . hCG is particularly important in primate reproduction where it has a similar effect to LH in stimulating the continued production of progesterone and oestrogens. This represents part of the system involved in foetal-maternal communication and . Primate blastocysts therefore produce hCG in relatively high concentrations during the first 3 months of pregnancy. hCG has also been suggested to play a role in defence of the embryo from the maternal immune system during the initial stages of pregnancy. In males hCG increases the growth of the foetal testes.

As hCG is only produced by embryonic cells, the presence of this hormone within maternal blood can be used for pregnancy confirmation.

Sex hormone synthesis, regulation, and function | …

In the present study, we found that estradiol stimulates mTOR in acute hippocampal slices through a signaling pathway involving TrkB receptor activation, ERK phosphorylation, and calpain activity. Specific inhibitors of each of these enzymes abrogated the increase in mTOR phosphorylation elicited by estradiol. These results are consistent with the recently identified mechanism linking BDNF-induced activation of the PI3K/Akt signaling cascade and stimulation of mTOR-dependent protein synthesis through calpain-2-mediated PTEN truncation () (see schematic in Figure ). In a previous study, we reported that BDNF and epidermal growth factor (EGF) specifically activated calpain-2 within dendritic spines through ERK-mediated phoshorylation (). Similarly, estradiol rapidly activates calpain in hippocampal neurons and this process has been implicated in estrogen modulation of synaptic plasticity (). The time course for estradiol regulation of ERK, Akt and mTOR phosphorylation as well as calpain activation, and PTEN degradation is in good agreement with that of BDNF-mediated regulation of the same sequence of events observed in our previous study (). Thus, estradiol enhanced ERK activity within 5min of application both in hippocampal slices and in cortical synaptoneurosomes, and this effect occurred in parallel to stimulation of calpain activity, as determined by the increase in SBDP. This was followed by a decrease in PTEN levels along with an increase in Akt and mTOR phosphorylation 15min after estradiol application. The activation of all these signaling proteins was transient, except for that of mTOR, which persisted for at least 1h after estradiol treatment. This time course is thus in good agreement with our previous study in which we showed that calpain, in addition to PTEN, causes the degradation of two of the negative regulators upstream of mTOR (and downstream of Akt), namely hamartin and tuberin ().

Sex hormone effects; Sex hormone synthesis, regulation, and function

Activin is a glycoprotein that is produced within granulosa cells in females and sertoli cells in the male. Activin is thought to play an almost directly opposite role to that of inhibin and is involved in many physiological functions including stimulation of FSH synthesis and other roles including cell proliferation, cell differentiation, apoptosis and homeostasis.

The target tissue for activin in the male is the epididymis where it enhances spermatogenesis via increased FSH secretion. Activin also enhances the effect of LH on the testes.

In the female activin has an effect on the anterior pituitary gland, specifically on gonadotroph cells, resulting in increased FSH secretion. The increased concentrations of activin results in increased FSH binding on the female follicle and FSH-induced aromatisation (increased synthesis of oestrogens). Activin also enhances the action of LH in the ovary.

A further non-reproductive role of activin is it's role in skin lesions where it is thought to stimulate keratinocytes.