Evidence map›Paper›PMID 20647494›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2010

17beta-estradiol rapidly enhances bradykinin signaling in primary sensory neurons in vitro and in vivo.

Matthew P Rowan, Kelly A Berg, Stephen B Milam, Nathan A Jeske, James L Roberts, Kenneth M Hargreaves, William P Clarke

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Functional selectivity of kappa opioid receptor agonists in peripheral sensory neurons.The Journal of pharmacology and experimental therapeutics · 2015
    Article
  7. Article
  8. Article
  9. Sex and the migraine brain.Neurobiology of disease · 2014
    Review
  10. Article
  11. Review
  12. Review
  13. Article
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  15. 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

7 authors at 3 institutions in 2 countries.

Matthew P RowanDepartment of Pharmacology, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.
Kelly A Berg
Stephen B Milam
Nathan A Jeske
James L Roberts
Kenneth M Hargreaves
William P Clarke
The University of Texas Health Science Center at San Antonio · USAmerican Association of Endodontists · USNational Medical Research Center of Dentistry and Maxillofacial Surgery · RU

Funding

Institutional Research Training GrantT32DE014318 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Kenneth M Hargreaves · 2002 to 2026
$12.1M
ESTROGEN MODULATION OF HUMAN NOCICEPTORSR01NS058655 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HARGREAVES, KENNETH M · 2008 to 2012
$1.6M
AKAP MODULATES TRPV1 PHOSPHORYLATION AND SENSITIZATIONR01NS061884 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JESKE, NATHANIEL AARON · 2008 to 2011
$1.3M
Estrogen regulation of inflammatory mediator signalingR01NS055835 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARKE, WILLIAM P · 2008 to 2011
$1.3M
NIDCR NIH HHS T32 DE014318NIDCR NIH HHS T32DE14318NINDS NIH HHS R01 NS055835NINDS NIH HHS R01-NS055835NINDS NIH HHS R01 NS058655NINDS NIH HHS R01-NS058655NINDS NIH HHS R01 NS061884NINDS NIH HHS R01-NS061884
6 · The paper itself

Abstract

Many studies have demonstrated that premenopausal women are at increased risk for various pain disorders. Pain-sensing neurons, termed "nociceptors," in the trigeminal ganglia (TG) and dorsal root ganglia (DRG) express receptors for inflammatory mediators and noxious physical stimuli and transmit signals for central processing of pain sensation. Estrogen receptors (ERs) are also expressed on nociceptors in the TG and DRG, and there is ample literature to suggest that activation of ERs can influence pain mechanisms. However, the mechanism for ER modulation of nociceptor activity is incompletely understood. The aim of this study was to characterize the effect of 17β-estradiol (17β-E(2)) on signaling of the inflammatory mediator bradykinin (BK) in primary cultures of rat sensory neurons and a behavioral model of thermal allodynia in rats. Here, we show that exposure to 17β-E(2) rapidly (within 15 min) enhanced responses to BK in vitro and in vivo. The 17β-E(2)-mediated enhancement of BK signaling was not blocked by the transcription inhibitor anisomycin and was mediated by a membrane-associated ER. The effect of 17β-E(2) to enhance BK responses required activation of β1-containing, RGD-binding integrins. These data show that 17β-E(2) rapidly enhances inflammatory mediator responses both in vitro and in vivo and suggest that 17β-E(2) acting at primary sensory pain neurons may participate in regulating the sensitivity of women to painful stimuli.

Indexed as

AnimalsAnisomycinBehavior, AnimalBradykininCells, CulturedEstradiolFemaleGanglia, SpinalInositol PhosphatesIntegrinsMaleNerve EndingsNucleic Acid Synthesis InhibitorsPainRatsRats, Sprague-DawleyAnisomycinBradykininEstradiolInositol PhosphatesIntegrinsNucleic Acid Synthesis InhibitorsType C Phospholipases

Identifiers

PMID20647494
PMCPMC2957773
OpenAlexW2143049356

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.