Evidence map›Paper›PMID 15843609›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Role of glucocorticoids and cAMP-mediated repression in limiting corticotropin-releasing hormone transcription during stress.

Jack D Shepard, Ying Liu, Paolo Sassone-Corsi, Greti Aguilera

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A users guide to HPA axis research.Physiology & behavior · 2017
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Novel aspects of glucocorticoid actions.Journal of neuroendocrinology · 2014
    Review
  10. Article
  11. Article
  12. Transcriptional regulation of episodic glucocorticoid secretion.Molecular and cellular endocrinology · 2013
    Review
  13. Article
  14. The molecular physiology of CRH neurons.Frontiers in neuroendocrinology · 2012
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Jack D ShepardSection on Endocrine Physiology, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20891, USA.
Ying Liu
Paolo Sassone-Corsi
Greti Aguilera
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USInstitut de génétique et de biologie moléculaire et cellulaire · FR

Funding

Neuroendocrine Control Of The Stress ResponseZIAHD000631 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI AGUILERA, GRETI · 2009 to 2014
$4.0M
NEUROENDOCRINE CONTROL OF THE STRESS RESPONSEZ01HD000631 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI AGUILERA, GRETI · 1990 to 2008
$2.2M
6 · The paper itself

Abstract

The role of glucocorticoids and the repressor isoform of cAMP response element (CRE) modulator (CREM), inducible cAMP early repressor (ICER), in limiting corticotropin-releasing hormone (CRH) transcription during restraint stress were examined in both intact and adrenalectomized rats receiving glucocorticoid replacement. CRH primary transcript, measured by intronic in situ hybridization, increased after 30 min of restraint and returned to basal levels by 90 min, despite the persistent stressor. The decline was independent of circulating glucocorticoids, because adrenalectomized rats displayed an identical pattern. ICER mRNA in the hypothalamic paraventricular nucleus (PVN) increased after 30 min and remained elevated for up to 4 h in a glucocorticoid-independent manner. Western blot and electrophoretic mobility shift assay analyses showed increases in endogenous ICER in the PVN of rats subjected to restraint stress for 3 h. Chromatin immunoprecipitation assays showed the recruitment of CREM by the CRH CRE in conjunction with decreases in RNA polymerase II (Pol II) binding in the PVN region of rats restrained for 3 h. These data show that stress-induced glucocorticoids do not mediate the limitation of CRH transcription. Furthermore, the ability of CREM to bind the CRH CRE and the time relationship between elevated CREM and reduced Pol II recruitment by the CRH promoter suggest that inhibitory isoforms of CREM induced during stress contribute to the decline in CRH gene transcription during persistent stimulation.

Indexed as

Adrenal Cortex HormonesAdrenalectomyAnalysis of VarianceAnimalsBlotting, WesternChromatin ImmunoprecipitationCorticotropin-Releasing HormoneCyclic AMP Response Element ModulatorElectrophoretic Mobility Shift AssayGene Expression RegulationGlucocorticoidsIn Situ HybridizationMaleParaventricular Hypothalamic NucleusRatsRats, Sprague-DawleyAdrenal Cortex HormonesCorticotropin-Releasing HormoneCrem protein, ratCyclic AMP Response Element ModulatorGlucocorticoidsRNA, Heterogeneous NuclearRNA, Messenger

Identifiers

PMID15843609
PMCPMC6724949
OpenAlexW2016200185

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.