Effects of estradiol on regulation of corticotropin-releasing factor gene and interleukin-6 production via estrogen receptor type β in hypothalamic 4B cells

Ogura, Eriko; Kageyama, Kazunori; Hanada, Ken‐ichi; Kasckow, John; Suda, Toshio

doi:10.1016/j.peptides.2007.11.007

Cited by 26 publications

(23 citation statements)

References 46 publications

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“…expression lev- els of eRa are very low in 4B cells, although they are highly expressed in the hypothalamic tissue (Fig. 6) [40]. The subtype of the dominant eR is eRb in hypothalamic 4B cells.…”

Section: Involvement Of Estrogen On Crf Gene Transcriptionmentioning

confidence: 86%

Regulatory Mechanisms Underlying Corticotropin-Releasing Factor Gene Expression in the Hypothalam

Kageyama

Suda

2009

Endocr J

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Abstract. The hypothalamic-pituitary-adrenal (HPa) axis is activated under various stressors. Corticotropin-releasing factor (CRF) plays a central role in controlling stress response, and regulating the HPa axis. CRF, produced in the hypothalamic paraventricular nucleus (PVN), stimulates adrenocorticotropic hormone (aCTH) production via CRF receptor type 1 (CRF 1 receptor) from the corticotrophs of the anterior pituitary (aP). Cyclic amP (camP)-protein kinase a (PKa) pathway takes a main role in stimulating CRF gene transcription. Forskolin and pituitary adenylate cyclaseactivating polypeptide (PaCaP) stimulate adenylate cyclase, intracellular camP production, and then CRF and arginine vasopressin (aVP) gene expression in hypothalamic 4B cells. Interleukin (IL)-6, produced in the PVN, both directly and indirectly stimulates CRF and aVP gene expression. estradiol may enhance the activation of CRF gene expression in response to stress. The HPa axis is regulated by a negative feedback mechanism, because glucocorticoids inhibit both CRF production in the hypothalamic PVN and aCTH production in the pituitary. Hypothalamic parvocellular neurons in the PVN are known to express glucocorticoid receptors, and glucocorticoids are able to regulate CRF gene transcription and expression levels directly in the PVN. glucocorticoids-dependent repression of camP-stimulated CRF promoter activity is mainly localized to promoter sequences between -278 and -233 bp. Both negative glucocorticoid regulatory element (ngRe) and serum response element (SRe) are involved in the repression of the CRF gene in the hypothalamic cells. Stimulation of crF gene in the hypothalamus Involvement of cAMP on CRF gene transcriptionCyclic amP (camP)-protein kinase a (PKa) pathway takes a main role in stimulating CRF synthesis [3][4][5]. There are several candidates for activating CRF neurons. For example, pituitary adenylate cyclase-activating polypeptide (PaCaP), a member of the secretin/glucagon/vasoactive intestinal peptide (VIP) family, is one of the putative hormones. Both PaCaP and the PaCaP-selective PaCaP receptor type 1 (PaC1 receptor) are known to be highly expressed in the hypothalamus, including the parvocellular and magnocellular subdivisions of the PVN, and the supraoptic nucleus (SON) [6,7]. PaCaP has shown to stimulate camP production in the aP [8]. PaCaP also increases CRF mRNa levels in the parvocellular region of the PVN, suggesting that PaCaP is involved in the positive regulation of CRF gene expression [9].

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Section: Involvement Of Estrogen On Crf Gene Transcriptionmentioning

confidence: 86%

Regulatory Mechanisms Underlying Corticotropin-Releasing Factor Gene Expression in the Hypothalam

Kageyama

Suda

2009

Endocr J

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“…Moreover, the drop in E 2 concentrations after PE is accompanied by a drop in ACTH concentrations, suggesting that the stimulatory effect of E 2 on corticotroph cells begins to diminish. In studies conducted in rat models and cell culture, it has been demonstrated that E 2 increases POMC mRNA synthesis (Ochedalski et al 2007) and acts upon the paraventricular nucleus stimulating the release of the corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) (Greer et al 1986;Ogura et al 2008;Panagiotakopoulos and Neigh Figure 4. Cortisol concentrations during the oestrous cycle in the female dog in negative and positive photoperiods.…”

Section: Discussionmentioning

confidence: 99%

“…Although several reports on the effect of E 2 on the HPA axis performed in cell cultures and animal models (rats, sheep) are available (McCormick et al 1998;Ochedalski et al 2007;Ogura et al 2008;Kageyama and Suda 2009;Weiser and Handa 2009;Handa and Weiser 2014;van Lier et al 2014), the mechanisms have not yet been fully elucidated. In general, it has been proposed that E 2 could exert a stimulatory effect on the hypothalamus, the corticotroph cells or the adrenal gland cortex (by stimulating CRH secretion or inhibiting glucocorticoid feedback, or stimulating ACTH synthesis or cortisol synthesis/secretion) (Burgess and Handa 1993;Carey et al 1995;McCormick et al 1998;Lo et al 2000;van Lier et al 2003b;Ochedalski et al 2007; Kageyama and Suda 2009;Weiser and Handa 2009;Handa and Weiser 2014;Panagiotakopoulos and Neigh 2014).…”

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confidence: 99%

Plasma ACTH, α-MSH and cortisol variations in the dog during the oestrous cycle in different photoperiods

Gallelli¹,

Monachesi²,

Miceli³

et al. 2015

Vet. Med. - Czech

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ABSTRACT:The hypothalamic-pituitary-adrenal axis (HPA) is a complex system regulated by multiple factors. Sexual dimorphism of this axis has been described in different species under physiological conditions and it has been proposed that sexual hormones could have an effect on it. There are only a few reports about sex-linked variations in HPA axis hormones in the dog. Thus, studying the impact of sexual hormones on the HPA axis would broaden the knowledge about its function in this species. Therefore, the objective of this study was to determine whether there are variations in HPA plasma hormones (ACTH, alfa-melanocyte-stimulating hormone [α-MSH] and cortisol) according to the sex and photoperiod (positive or negative photoperiod were considered when the duration of the light hours of the day was more than 12 or less than 12, respectively) under basal conditions (like anoestrus) and throughout the oestrous cycle in the female dog. The population under study consisted of 11 intact female and 14 intact male dogs. Under basal conditions neither ACTH nor α-MSH concentrations showed differences between sexes and different photoperiods. Cortisol showed greater values in the negative photoperiod than in the positive, both in females and males (P = 0.03 and P = 0.015, respectively). Throughout the oestrous cycle, all the studied hormones showed variations (P < 0.0001). The greatest concentrations of ACTH were observed at proestrus, while α-MSH and cortisol showed their greatest concentrations at oestrus. The three hormones decreased in diestrus. ACTH and cortisol concentrations were higher in the negative photoperiod (P = 0.04 and P < 0.0001, respectively), while α-MSH concentrations were higher in the positive photoperiod (P = 0.012). In the group of females oestradiol and progesterone correlated with ACTH (r = 0.75, P < 0.0001; r = 0.34, P < 0.01, respectively), α-MSH (r = 0.49, P < 0.0001; r = 0.52, P < 0.0001, respectively) and cortisol (r = 0.33, P < 0.01; r = 0.5, P < 0.0001, respectively). These results show that in females, HPA axis hormones vary during the oestrous cycle in relation to oestradiol and progesterone fluctuations. The ACTH, α-MSH and cortisol concentrations also showed differences between photoperiods in females, but only cortisol did so in males. These findings suggest that sexual hormones could have an effect on the HPA axis. Further research needs to be done to fully understand this interaction and the mechanisms involved.

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“…The lids were removed, and the vials were placed in an incubator (Memmert) at 60°C for 72 hours and then reweighed (dry weight). The percentage of water in each sample was then calculated using a previously published formula: 36,41 (100 × [(wet weight -dry weight)/wet weight]).…”

Section: Determination Of Brain Water Contentmentioning

confidence: 99%

“…54 In addition, a growing number of studies have reported antiinflammatory roles for ERb, such as neuroprotection after ischemia, 1,8,57 inhibition of microglial activity, 4 suppression of transcription, and decreased levels of IL-1b, IL-6, TNFa, and chemokine CCL2. 7,36 There are discrepancies in data among studies that used ER agonists versus genetically ER-deficient animals and studies that have used the agonists. Some reasons for the differences in these other results with those in our study might be differences in dose, formulation, the type and severity of injury, route of administration, time of using the agonists, and length of treatment.…”

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confidence: 99%

Contribution of estrogen receptors alpha and beta in the brain response to traumatic brain injury

Asl

Khaksari²,

Khachki

et al. 2013

JNS

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Object Although there is evidence that estradiol has neuroprotective effects after traumatic brain injury (TBI) in female rats, it is unclear which estrogen receptor (ER) subtype, ERα or ERβ, mediates this effect. The authors therefore examined the roles of the different ERs in this effect. Here the authors used the ERα selective agonist propyl pyrazole triol (PPT) and the ERβ selective agonist diarylpropionitrile (DPN) alone and in combination in female rats to investigate this question. Methods Before the ovariectomized animals were injured using the Marmarou TBI technique, they were randomly divided into the following 9 groups: control, sham, TBI, vehicle, E1 (physiological dose of 17-β estradiol), E2 (pharmacological dose of 17-β estradiol), PPT, DPN, and PPT+DPN. Levels of blood-brain barrier (BBB) disruption (5 hours) and water content (24 hours) were evaluated after TBI. In groups receiving drugs or vehicle, treatment was administered as a single dose intraperitoneally 30 minutes after induction of TBI. Results Results showed that brain edema or brain water content after TBI was lower (p < 0.001) in the E2, PPT, DPN, and PPT+DPN groups than it was in the vehicle group. After trauma, the Evans blue dye content or BBB permeability was significantly higher in the TBI and vehicle groups (p < 0.001) than in the E2, PPT, DPN, and PPT+DPN groups. The inhibitory effects of PPT+DPN on brain water content, neurological scores, and Evans blue dye content were the highest for all groups. Although both PPT and DPN increased neurological scores after TBI, PPT appears to be more effective in increasing neurological scores. Conclusions Neuroprotective effects of estradiol on brain edema, BBB permeability, and neurological scores are mediated through both ERα and ERβ. This may suggest a therapeutic potential in the brain trauma for ER-specific agonists.

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Effects of estradiol on regulation of corticotropin-releasing factor gene and interleukin-6 production via estrogen receptor type β in hypothalamic 4B cells

Cited by 26 publications

References 46 publications

Regulatory Mechanisms Underlying Corticotropin-Releasing Factor Gene Expression in the Hypothalam

Regulatory Mechanisms Underlying Corticotropin-Releasing Factor Gene Expression in the Hypothalam

Plasma ACTH, α-MSH and cortisol variations in the dog during the oestrous cycle in different photoperiods

Contribution of estrogen receptors alpha and beta in the brain response to traumatic brain injury

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