Evidence map›Paper›PMID 26963472›Full record

ArticleEndocrinology2016

Centrally Synthesized Estradiol Is a Potent Anti-Inflammatory in the Injured Zebra Finch Brain.

Alyssa L Pedersen, Lars H Nelson, Colin J Saldanha

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.8field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Frontiers in neural circuits · 2025
    Article
  2. Review
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  5. Article
  6. Brain-derived estrogen and neural function.Neuroscience and biobehavioral reviews · 2022
    Review
  7. Review
  8. Glial estradiol synthesis after brain injury.Current opinion in endocrine and metabolic research · 2021
    Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
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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

3 authors at 1 institution in 1 country.

Alyssa L PedersenDepartment of Biology, Behavior, Cognition, and Neuroscience Program and The Center for Behavioral Neuroscience, American University, Washington, DC 20016.
Lars H NelsonDepartment of Biology, Behavior, Cognition, and Neuroscience Program and The Center for Behavioral Neuroscience, American University, Washington, DC 20016.
Colin J SaldanhaDepartment of Biology, Behavior, Cognition, and Neuroscience Program and The Center for Behavioral Neuroscience, American University, Washington, DC 20016.
American University · US

Funding

NIH HHS 042767NIH HHS 080585
6 · The paper itself

Abstract

In homeotherms, injury to the brain, such as a penetrating wound, increases microglial cytokine expression and astroglial aromatase (estrogen synthase). In songbirds, injury-induced synthesis of estrogens is neuroprotective as aromatase inhibition and replacement with estradiol (E2) exacerbates and mitigates the extent of damage, respectively. The influence of induced aromatization on inflammation, however, remains unstudied. We hypothesized that injury-induced aromatization, via E2 synthesis, may affect neuroinflammation after a penetrating brain injury. Using adult zebra finches, we first documented an increase in the transcription of cytokines but not aromatase, 2 hours after the injury. Twenty-four hours after the injury, however, aromatase was dramatically elevated and cytokine expression had returned to baseline, suggesting that aromatization may be involved in the decrease of cytokines and neuroinflammation. In two subsequent experiments, we tested the influence of the inhibition of induced aromatization and aromatase inhibition with concomitant central E2 replacement on the transcription of the cytokines TNF-α, IL-1β, and IL-6, the enzyme cyclooxygenase-2 (cox-2), and its product prostaglandin E2 (PGE2). Administration of fadrozole, an aromatase inhibitor, caused a sustained elevation of IL-1β in females and TNF-α, cox-2, and PGE2 in both sexes. This prolonged neuroinflammation appears to be due to a failure to synthesize E2 locally because intracranial E2 replacement lowered IL-1β in females, TNF-α in males, and cox-2 and PGE2 in both sexes. IL-6 was not affected by injury, aromatase inhibition, or E2 replacement in either sex. These data suggest that E2 synthesis after a penetrating brain injury is a potent and inducible anti-inflammatory signal, with specific modulation of discrete cytokine signaling.

Indexed as

AnimalsAromataseAromatase InhibitorsBrainBrain InjuriesCyclooxygenase 2DinoprostoneEstradiolFadrozoleFemaleFinchesInflammationInterleukin-1betaInterleukin-6MaleTumor Necrosis Factor-alphaAromataseAromatase InhibitorsCyclooxygenase 2DinoprostoneEstradiolFadrozoleInterleukin-1betaInterleukin-6Tumor Necrosis Factor-alpha

Identifiers

PMID26963472
PMCPMC4870876
OpenAlexW2294428446

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.