Vasoactive intestinal peptide (VIP) stimulates cortisol secretion from the H295 human adrenocortical tumour cell line via VPAC1 receptors

Nicol,; Cobb, V J; Williams, B C; Morley, Steven D.; Walker, S. W.; Mason, J. Ian

doi:10.1677/jme.0.0320869

Cited by 11 publications

(7 citation statements)

References 37 publications

(37 reference statements)

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“…Forskolin, an activator of adenylyl cyclase, produced a PRC similar to that of ACTH. In contrast, neither VIP nor CRH elicited a phase shift when administered at CT18, although both affect adrenal steroidogenesis via G s protein-coupled receptors (32,50). A more thorough examination of these peptides is warranted, yet these findings further support the specificity of MC2R activation by ACTH in resetting the adrenal clock.…”

Section: Discussionmentioning

confidence: 89%

“…Neither the period nor the amplitude of the rhythm was affected by ACTH. The magnitude of the phase shift at CT18 was concentration-dependent and peptide-specific; responses were not observed following CRH 1-41 or VIP 1-28, peptides that bind receptors in the adrenal cortex to elicit steroid responses (32,50). Because ACTH is degraded within 2 h in adrenal tissue culture (3), treatment at CTs separated by 4 h should provide "pulse-like" exposure to ACTH; however, the resolution of the PRC could be masked by lingering bioactivity.…”

Section: Discussionmentioning

confidence: 94%

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Phase-dependent resetting of the adrenal clock by ACTH in vitro

Yoder

Brandeland

Engeland

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Yoder JM, Brandeland M, Engeland WC. Phase-dependent resetting of the adrenal clock by ACTH in vitro. Am J Physiol Regul Integr Comp Physiol 306: R387-R393, 2014. First published January 29, 2014 doi:10.1152/ajpregu.00519.2013The adrenal cortex has a molecular clock that generates circadian rhythms in glucocorticoids, yet how the clock is synchronized to the external environment is unknown. Using mPER2::Luciferase (mPER2Luc) knockin mice, in which luciferase is rhythmically expressed under the control of the mouse Per2 clock gene, we hypothesized that ACTH transmits entrainment signals to the adrenal. Adrenal explants were administered ACTH at different phases of the mPER2Luc rhythm. Treatment with ACTH 1-39 produced a phase delay that was phase-dependent, with a maximum at circadian time (CT)18; ACTH did not alter the period or amplitude of the rhythm. Forskolin produced a parallel response, suggesting that the phase delay was cAMP-mediated. The response to ACTH was concentration-dependent and peptide-specific. Pulse administration (60 min) of ACTH 1-39 also produced phase delays restricted to late CTs. In contrast to ACTH 1-39, other ACTH fragments, including ␣-melanocyte-stimulating hormone, which do not activate the melanocortin 2 (MC2/ACTH) receptor, had no effect. The finding that ACTH in vitro phase delays the adrenal mPER2luc rhythm in a monophasic fashion argues for ACTH as a key resetter, but not the sole entrainer, of the adrenal clock. adrenal clock; adrenocorticotropic hormone; nonphotic entrainment THE HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) axis is characterized by a robust circadian variation in glucocorticoids. This rhythm is paralleled by rhythms in plasma ACTH (6), and adrenal sensitivity to ACTH (10) mediated, in part, by sympathetic activity (49). Rhythmic ACTH secretion is regulated by corticotropin-releasing hormone (CRH) from the hypothalamic paraventricular nucleus (PVN) (6). Circadian timing is dependent on a clock in the suprachiasmatic nucleus (SCN) (41) that is reset daily by photic information transmitted from the retina (28) with SCN neurons relaying these signals to the PVN (19). This mechanism guarantees that glucocorticoid rhythms are entrained to the daily light-dark (LD) cycle.A molecular clock exists in the SCN (39) and peripheral tissues (12), including the adrenal (4). The clock consists of interlocking feedback loops of gene transcription and translation (39). The "positive" limb involves CLOCK and BMAL1, which heterodimerize and activate transcription of period genes, Per1 and Per2, and cryptochrome genes, Cry1 and Cry2. The Per and Cry transcripts increase with the protein products, PER and CRY, functioning as the "negative limb" by forming heterodimers that act on the CLOCK:BMAL1 complex to repress their own transcription. The feedback loops are self-regulating with an ϳ24-h periodicity.The adrenal clock controls steroidogenesis by gating sensitivity to ACTH. In Per2/Cry1 mutant mice that lack a functioning clock, rhythms in adrenal sensitivity are absent and the cortico...

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 94%

Phase-dependent resetting of the adrenal clock by ACTH in vitro

Yoder

Brandeland

Engeland

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Li and Wang, 2005), functional corticotrophin-releasing hormone (CRH) receptors (Willenberg et al, 2005) and respond to forskolin and isobutyl methylxanthine cyclic AMP induction and dibutyryl cyclic AMP by stimulated corticosteroid synthesis (Xu et al, 2003). They also respond to angiotensin II by production of aldosterone (Kau et al, 2005), vasoactive intestinal peptide (VIP) by production of cortisol (Nicol et al, 2004), have functional atrial natriuretic peptide (ANP) receptors (Bodart et al, 1996), have functional luteinizing hormone (LH)/chorionic gonadotrophin (hCG) receptors (Rao et al, 2004) and respond to activin A (activins and inhibins are related glycoproteins that modulate pituitary follicle stimulating hormone (FSH) and consequently sex steroid production) by decreased sex steroid secretion (Vanttinen et al, 2003). H295R cells are also reported to respond to tumour necrosis factor which increases steroidogenesis (Mikhaylova et al, 2007) and epidermal growth factor and prostaglandins (Watanabe et al, 2006).…”

Section: Identifying Molecular Targets and Mechanismsmentioning

confidence: 99%

Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis

Harvey

Everett

Springall

2007

J of Applied Toxicology

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The adrenal is the most common toxicological target organ in the endocrine system in vivo and yet it is neglected in regulatory endocrine disruption screening and testing. There has been a recent marked increase in interest in adrenal toxicity, but there are no standardised approaches for assessment. Consequently, a strategy is proposed to evaluate adrenocortical toxicity. Human adrenal conditions are reviewed and adrenocortical suppression, known to have been iatrogenically induced leading to Addisonian crisis and death, is identified as the toxicological hazard of most concern. The consequences of inhibition of key steroidogenic enzymes and the possible toxicological modulation of other adrenal conditions are also highlighted. The proposed strategy involves an in vivo rodent adrenal competency test based on ACTH challenge to specifically examine adrenocortical suppression. The H295R human adrenocortical carcinoma cell line is also proposed to identify molecular targets, and is useful for measuring steroids, enzymes or gene expression. Hypothalamo-pituitary-adrenal endocrinology relevant to rodent and human toxicology is reviewed (with an emphasis on multi-endocrine axis effects on the adrenal and also how the adrenal affects a variety of other hormones) and the endocrinology of the H295R cell line is also described. Chemicals known to induce adrenocortical toxicity are reviewed and over 60 examples of compounds and their confirmed steroidogenic targets are presented, with much of this work published very recently using H295R cell systems. In proposing a strategy for adrenocortical toxicity assessment, the outlined techniques will provide hazard assessment data but it will be regulatory agencies that must consider the significance of such data in risk extrapolation models. The cases of etomindate and aminoglutethimide induced adrenal suppression are clearly documented examples of iatrogenic adrenal toxicity in humans. Environmentally, sentinel species, such as fish, have also shown evidence of adrenal endocrine disruption attributed to exposure to chemicals. The extent of human sub-clinical adrenal effects from environmental chemical exposures is unknown, and the extent to which environmental chemicals may act as a contributory factor to human adrenal conditions following chronic low-level exposures will remain unknown unless purposefully studied.

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“…PACAP is neurotransmitter that stimulates cortisol secretion in adrenocortical cells when it binds to its receptor PAC 1 [18]. PAC 1 antagonism stimulates the hypothalamic–pituitary–adrenal (HPA) axis and attenuates corticosterone release in rodents [19].…”

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confidence: 99%

Placental Epigenetic Patterning of Glucocorticoid Response Genes is Associated with Infant Neurodevelopment

et al. 2015

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Aim To determine associations between methylation of NR3C1, HSD11B2, FKBP5 and ADCYAP1R1 and newborn neurobehavioral outcomes. Methods In 537 newborns, placental methylation was quantified using bisulfite pyrosequencing. Profiles of neurobehavior were derived via the Neonatal Intensive Care Unit Network Neurobehavioral Scales. Using exploratory factor analysis, the relationships between methylation factor scores and neurobehavioral profiles were examined. Results Increased scores of the factor characterized by NR3C1 methylation were associated with membership in a reactive, poorly regulated profile (odds ratio: 1.47; 95% CI: 1.00–2.18), while increased scores of the factor characterized by HSD11B2 methylation reduced this risk. Conclusion These results suggest that coordinated regulation of these genes influences neurobehavior and demonstrates the importance of examining these alterations in a harmonized fashion.

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Vasoactive intestinal peptide (VIP) stimulates cortisol secretion from the H295 human adrenocortical tumour cell line via VPAC1 receptors

Cited by 11 publications

References 37 publications

Phase-dependent resetting of the adrenal clock by ACTH in vitro

Phase-dependent resetting of the adrenal clock by ACTH in vitro

Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis

Placental Epigenetic Patterning of Glucocorticoid Response Genes is Associated with Infant Neurodevelopment

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