Regulation of vertebrate corticotropin-releasing factor genes

Yao, Meng; Denver, Robert J.

doi:10.1016/j.ygcen.2007.01.046

Cited by 81 publications

(70 citation statements)

References 217 publications

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“…GR has been shown to be a negative regulator of CRH via binding to the promoter region of the CRH gene to inhibit transcription. 134 Increases in GR expression observed together with an increase in CRH following unpredictable ELS, suggest a dysfunction in the regulatory relationship between GR and CRH within the CeA. This mechanistic difference is likely a product of the complex interaction between the type of stress experienced and sex-related vulnerabilities.…”

Section: Epigenetic Mechanisms That Contribute To Irritable Bowel Synmentioning

confidence: 99%

Mechanisms of Stress-induced Visceral Pain

Meerveld

Johnson

2018

J Neurogastroenterol Motil

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Evidence suggests that long-term stress facilitates visceral pain through sensitization of pain pathways and promotes chronic visceral pain disorders such as the irritable bowel syndrome (IBS). This review will describe the importance of stress in exacerbating IBS-induced abdominal pain. Additionally, we will briefly review our understanding of the activation of the hypothalamic-pituitary-adrenal axis by both chronic adult stress and following early life stress in the pathogenesis of IBS. The review will focus on the glucocorticoid receptor and corticotropin-releasing hormone-mediated mechanisms in the amygdala involved in stress-induced visceral hypersensitivity. One potential mechanism underlying persistent effects of stress on visceral sensitivity could be epigenetic modulation of gene expression. While there are relatively few studies examining epigenetically mediated mechanisms involved in stress-induced visceral nociception, alterations in DNA methylation and histone acetylation patterns within the brain, have been linked to alterations in nociceptive signaling via increased expression of pro-nociceptive neurotransmitters. This review will discuss the latest studies investigating the long-term effects of stress on visceral sensitivity. Additionally, we will critically review the importance of experimental models of adult stress and early life stress in enhancing our understanding of the basic molecular mechanisms of nociceptive processing. Taken together, the complex clinical phenotype makes recapitulating IBS in rodent models extremely challenging. However, an aim of this review will be to describe how the use of rodent models of adult stress, early life stress (ELS), and a dysregulated HPA axis has improved our understanding of stress in the pathophysiology of IBS. Pathophysiology of Irritable Bowel Syndrome: Activation of the Brain-Gut AxisEvidence from clinical and basic research points to dysregulation of the bidirectional communication between the brain-gut axis in IBS. 21 The brain-gut axis represents a dynamic interplay between central circuits and peripheral mechanisms. The messengers of this complex circuit include neural, endocrine, metabolic, and immune mediators that are activated by central factors such as stress (Fig. 1). Although IBS is not an inflammatory disorder, the immune system plays a role in the pathogenesis of IBS in at least a subset of patients and likely contributes to the etiology of IBS symptoms. 22,23 A subset of IBS patients display a low grade chronic inflammation, and there is also evidence that following an enteric infection and combined with stressful life events, there is an increased risk of developed post-infectious IBS. [24][25][26][27] Clearly, the immune system and inflammatory processes are modulated by the HPA and autonomic nervous systems. In support, IBS patients also show increased number and reactivity of mast cells. 28,29 Data from peripheral blood mononuclear cells, as well as in mucosal biopsies, from IBS patients show that cytokines levels including TNF-α...

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Section: Epigenetic Mechanisms That Contribute To Irritable Bowel Synmentioning

confidence: 99%

Mechanisms of Stress-induced Visceral Pain

Meerveld

Johnson

2018

J Neurogastroenterol Motil

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“…In mammals, low levels of glucocorticoids acting at MR in the limbic system modulate basal (diurnal) HPA axis activity, whereas high levels of glucocorticoids suppress stressorinduced activation of the HPA axis in part through GR-mediated suppression of crf transcript abundance in the POA (Yao & Denver 2007). In fish, the relative contribution of GR and MR to HPI axis regulation is less clear.…”

Section: Hsd11b2 and Hpi Axis Regulationmentioning

confidence: 99%

“…In mammals, diurnal hypothalamus pituitary adrenal (HPA) axis activity is regulated by glucocorticoid-negative feedback acting through the highaffinity mineralocorticoid receptor (MR), whereas stressor levels of glucocorticoids exert negative feedback by binding to the lower affinity glucocorticoid receptor (GR; Yao & Denver 2007). In teleosts, we recently showed that GR is involved in the cortisol response to stress (Alderman et al 2012), but the mechanism involved in the negative feedback regulation of cortisol is not known.…”

Section: Introductionmentioning

confidence: 99%

11β-Hydroxysteroid dehydrogenase type 2 in zebrafish brain: a functional role in hypothalamus-pituitary-interrenal axis regulation

Alderman

Vijayan

2012

Journal of Endocrinology

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The type 2, 11b-hydroxysteroid dehydrogenase (Hsd11b2) converts active glucocorticoids to their inactive derivatives (e.g. cortisol to cortisone). In most vertebrates, Hsd11b2 is essential for conferring aldosterone-specific actions in mineralocorticoid target tissues and for protecting glucocorticoid-sensitive tissues during stress. However, teleosts do not synthesize aldosterone, and the function of Hsd11b2 is poorly defined. The distribution of Hsd11b2 in nonmammalian brain is also largely unexplored. We tested the hypothesis that modulation of brain Hsd11b2 activity is involved in stressor-mediated cortisol regulation in zebrafish (Danio rerio). In adult zebrafish, the stress effect on Hsd11b2 expression in the brain was tested using acute air exposure followed by recovery over a 24-h period. hsd11b2 transcripts were found in nearly all peripheral tissues examined, and a spatial map of its mRNA abundance in unstressed zebrafish brain revealed extensive distribution. Stressor exposure increased the conversion of 3 H-cortisol to 3 H-cortisone indicating enhanced Hsd11b2 activity in zebrafish brain. Promoter analysis of zebrafish hsd11b2 gene revealed putative sites for cortisol-mediated transcriptional regulation of this gene. Furthermore, inhibition of Hsd11b2 activity by 18b-glycyrrhetinic acid resulted in elevated whole-body cortisol levels and preoptic area mRNA abundance of corticotropin-releasing factor and mineralocorticoid receptor. Taken together, our results underscore an important role for brain Hsd11b2 involvement in the negative feedback regulation of cortisol poststress in zebrafish.

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“…Computer analysis of the proximal CRF promoter reveals several possible binding sites for transcriptional factors, such as camP-response element (CRe), activator protein 1 (aP-1) protein (Fos/Jun) binding sites, half glucocorticoid regulatory element (gRe), and half estrogen-responsive element (eRe) [10]. Forskolin or PaCaP stimulates adenylate cyclase, and then increases intracellular camP levels in hypothalamic 4B cells (Fig.…”

Section: Involvement Of Camp On Crf Gene Transcriptionmentioning

confidence: 99%

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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Regulation of vertebrate corticotropin-releasing factor genes

Cited by 81 publications

References 217 publications

Mechanisms of Stress-induced Visceral Pain

Mechanisms of Stress-induced Visceral Pain

11β-Hydroxysteroid dehydrogenase type 2 in zebrafish brain: a functional role in hypothalamus-pituitary-interrenal axis regulation

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

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