Rapid signaling by steroid receptors

Levin, Ellis R.

doi:10.1152/ajpregu.90605.2008

Cited by 88 publications

(58 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, multiple studies have proven involvement of G-proteins and the signal-regulated kinase-CREB pathway. Importantly, these same pathways are also activated by rapid signalling of other steroid receptors, such as the oestrogen receptor (ER), androgen receptor (AR), progesterone receptor (PR; reviewed in (Hammes & Levin 2007, Vasudevan & Pfaff 2007, Levin 2008) and by rapid aldosterone signalling through the MR in peripheral tissues (Grossmann & Gekle 2009). Information gathered in these related fields could serve as an important guideline for investigation of the signalling partners of corticosteroids in the brain.…”

Section: Discussionmentioning

confidence: 99%

Rapid non-genomic effects of corticosteroids and their role in the central stress response

Groeneweg¹,

Karst²,

Kloet³

et al. 2011

Journal of Endocrinology

364

269

View full text Add to dashboard Cite

In response to a stressful encounter, the brain activates a comprehensive stress system that engages the organism in an adaptive response to the threatening situation. This stress system acts on multiple peripheral tissues and feeds back to the brain; one of its key players is the family of corticosteroid hormones. Corticosteroids affect brain functioning through both delayed, genomic and rapid, non-genomic mechanisms. The latter mode of action has long been known, but it is only in recent years that the physiological basis in the brain is beginning to be unravelled. We now know that corticosteroids exert rapid, non-genomic effects on the excitability and activation of neurons in (amongst others) the hypothalamus, hippocampus, amygdala and prefrontal cortex. In addition, corticosteroids affect cognition, adaptive behaviour and neuroendocrine output within minutes. Knowledge on the identity of the receptors and secondary pathways mediating the non-genomic effects of corticosteroids on a cellular level is accumulating. Interestingly, in many cases, an essential role for the 'classical' mineralocorticoid and glucocorticoid receptors in a novel membrane-associated mechanism is found. Here, we systematically review the recent literature on non-genomic actions of corticosteroids on neuronal activity and functioning in selected limbic brain targets. Further, we discuss the relevance of these permissive effects for cognition and neuroendocrine control, and the integration of this novel mode of action into the complex balanced pattern of stress effects in the brain.

show abstract

Section: Discussionmentioning

confidence: 99%

Rapid non-genomic effects of corticosteroids and their role in the central stress response

Groeneweg¹,

Karst²,

Kloet³

et al. 2011

Journal of Endocrinology

364

269

View full text Add to dashboard Cite

show abstract

“…Fate of Progesterone: Within a few minutes after secretion, almost all the progesterone is degraded to other steroids that have no progestational effect (Levin, 2008). As with the estrogens, the liver is especially important for this metabolic degradation.…”

Section: Functions Of the Liver In Sex Hormones Degradationmentioning

confidence: 99%

A review on haematological profile in menstruating, pre-menopausal and menopausal women

Obeagu¹,

Obeagu²

2016

Int. J. Adv. Res. Biol. Sci.

View full text Add to dashboard Cite

In females, the reproductive age is characterized by the onset of menstruation called menarche and ceases with the onset of menopause. The female reproductive cycles are controlled by various hormones and these hormones are known as female hormonal system. The female sexual cycle is the cycle of natural changes that occurs in the uterus and ovary as an essential part of making sexual reproduction possible. Its timing is governed by endogenous biological cycles. During the first few days of each monthly female sexual cycle, the concentrations of both FSH and LH secreted by the anterior pituitary gland increase slightly to moderately, with the increase in FSH slightly greater than that of LH and preceding it by a few days. These hormones, especially FSH, cause accelerated growth of 6 to 12 primary follicles each month. Menstruation is the principal cause of iron loss in women. The menstrual period is associated to the rupture of blood vessels which irrigate the superficial layer of the endometrium. Platelets constitute the first haemostatic component that mobilizes in order to interrupt the bleeding as vascular injury occurs. During menstruation, tremendous numbers of leukocytes are released along with the necrotic materials and blood. This is probable as a result of some substances released by the endometrial necrosis which causes the outflow of leukocytes during menstruation. The paper reviewed haematological profile menstruating women,premenopause women and menopause women.

show abstract

“…En effet, la signalisation membranaire du REα nécessite un ensemble de protéines différentes ou « signalosome » (Levin, 2008) dans lequel le GPR30 pourrait jouer un rôle particulier. Dans les cellules MCF-7, l'activation de Erk et l'expression de Fos par l'E2 ne serait possible qu'en présence du REα et du GPR30 (Albanito et al, 2007) sans connaitre le mécanisme de cette interaction.…”

Section: Le Gpr30 Un Récepteur Des Estrogènes ?unclassified

The DHEA metabolite 7β-hydroxy-epiandrosterone exerts anti-estrogenic effects on breast cancer cell lines

et al. 2012

View full text Add to dashboard Cite

Titre : La 7β-hydroxy-épiandrostérone dans des modèles in vitro de cancer du sein : effets anti-estrogéniques et rôle des récepteurs des estrogènes. La 7β-hydroxy-épiandrostérone, stéroïde endogène dérivant de la DHEA, présente des propriétés antiinflammatoires. En effet, elle module la voie des prostaglandines (PGs) en inhibant la production de la PGE2 pro-inflammatoires et en augmentant la production de la 15-Deoxy-∆ 12,14 -PGJ2 cyto-protectrice in vivo et in vitro. Les faibles doses de 7β-hydroxy-épiandrostérone (1nM, 10nM, 100nM) pour lesquelles ces effets sont observés, suggèrent une liaison à un récepteur spécifique. L'inflammation et la production des PGs jouent un rôle important dans le développement et la prolifération des tumeurs mammaires estrogéno-dépendantes. Le 17β-estradiol (E2), en se fixant sur les récepteurs des estrogènes (REs), induit la production de PGE2 et la prolifération cellulaire dans ces cellules tumorales. De ce fait, notre objectif était de tester les effets de la 7β-hydroxy-épiandrostérone sur la prolifération (comptage avec exclusion au bleu trypan), le cycle cellulaire et l'apoptose (cytométrie de flux) dans les lignées cellulaires de cancer du sein MCF-7 (REα+, REβ+, GPR30+) et MDA-MB-231 (REα-, REβ+, GPR30+) et d'identifier une(des) cible(s) potentielle(s) dans ces cellules (transactivation) et dans des cellules négatives pour les REs nucléaires SKBr3 (GPR30+) (études de prolifération). Cette étude a montré que la 7β-hydroxy-épiandrostérone exerce des effets anti-estrogéniques dans les cellules MCF-7 et MDA-MB-231 associés à une inhibition de la prolifération et un arrêt du cycle cellulaire. Les études de transactivation et de prolifération avec les agonistes spécifiques des REs ont montré une interaction avec le REβ. De plus, les résultats des études de proliférations sur les trois lignées cellulaires suggèrent que la 7β-hydroxy-épiandrostérone pourrait également interagir avec le GPR30. Ces résultats indiquent que ce stéroïde androgène agit comme un anti-estrogène. De plus, c'est la première fois qu'un stéroïde androgène à faible dose montre une action anti-proliférative dans des lignées de cancers du sein. De études ultérieures restent à réaliser afin de mieux comprendre ces effets observés. Mots clés : 7β-hydroxy-épiandrostérone, récepteurs des estrogènes, lignées de carcinomes mammaires, prolifération, transactivationThe DHEA metabolite 7β-hydroxy-epiandrosterone exerts anti-estrogenic effects on breast cancer cell lines 7β-hydroxy-epiandrosterone, an endogenous androgenic derivative of DHEA, has previously been shown to exert anti-inflammatory action in vitro and in vivo via a shift from prostaglandin E2 (PGE2) to 15-deoxy-∆ 12,14 -PGJ2 production. This modulation in prostaglandin production was obtained with low concentrations of 7β-hydroxy-epiandrosterone (1-100 nM) and suggested that it might act through a specific receptor. Inflammation and prostaglandin synthesis is important in the development and survival of estrogendependent mammary cancers. Estrogen induced PGE2 ...

show abstract

Rapid signaling by steroid receptors

Cited by 88 publications

References 98 publications

Rapid non-genomic effects of corticosteroids and their role in the central stress response

Rapid non-genomic effects of corticosteroids and their role in the central stress response

A review on haematological profile in menstruating, pre-menopausal and menopausal women

The DHEA metabolite 7β-hydroxy-epiandrosterone exerts anti-estrogenic effects on breast cancer cell lines

Contact Info

Product

Resources

About