Evidence map›Paper›PMID 19657024›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Estrogen induces caspase-dependent cell death during hypothalamic development.

Elizabeth M Waters, Richard B Simerly

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

54 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. The Role of Estrogen in Brain MicroRNAs Regulation.Advanced pharmaceutical bulletin · 2024
    Review
  3. Epigenetic Mechanisms of Brain Sexual Differentiation.Cold Spring Harbor perspectives in biology · 2022
    Review
  4. Article
  5. Oestrogenic Regulation of Mitochondrial Dynamics.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Role of 17Journal of oncology · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Incorporating Sex As a Biological Variable in Neuropsychiatric Research: Where Are We Now and Where Should We Be?Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Article
  20. Review
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

2 authors at 2 institutions in 1 country.

Elizabeth M WatersHarold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York 10065, USA. e.waters@rockefeller.edu
Richard B Simerly
Children's Hospital of Los Angeles · USRockefeller University · US

Funding

Development of Sexually Dimorphic Forebrian PathwaysR01NS037952 · NINDS · OREGON HEALTH AND SCIENCE UNIVERSITY · PI SIMERLY, RICHARD B · 1999 to 2009
$2.4M
NINDS NIH HHS R01 NS037952
6 · The paper itself

Abstract

The sexually dimorphic population of dopamine neurons in the anteroventral periventricular nucleus of the preoptic region of the hypothalamus (AVPV) develops postnatally under the influence of testosterone, which is aromatized to estrogen. There are fewer dopaminergic neurons labeled with tyrosine hydroxylase (TH) in the male AVPV than the female, and sex steroids determine this sex difference, yet the role of cell death in specifying numbers of dopaminergic neurons in the AVPV is unknown. Estradiol treatment of the AVPV, in vivo and in vitro, was used to manipulate TH-ir cell number. In vitro, concurrent treatment with the estrogen receptor antagonist ICI 182,780 rescued TH-ir cells. Cyclosporin A, an inhibitor of cell death dependent on the opening of a mitochondrial permeability transition pore also blocked TH-ir cell loss. In vivo, estradiol increased the number of apoptotic profiles, both TUNEL and Hoechst labeled nuclei, in the AVPV. This increased apoptosis was also dependent on the presence of the alpha form of the estrogen receptor. To test for caspase dependent TH-ir cell loss, the pancaspase inhibitor ZVAD (N-benzyloxycabonyl-Val-Ala-Asp-fluoromethylketone) was used to rescue TH-ir cells from estradiol-mediated reduction in number. Together, these data suggest that an intrinsic cell death pathway is activated by estrogen to regulate TH-ir cell number. Thus, in contrast to the more widespread neuroprotective actions of sex steroids in the mammalian nervous system, in the AVPV estrogen regulates dopaminergic neuron number through a caspase-dependent mechanism of apoptotic cell death.

Indexed as

AnimalsApoptosisCaspase InhibitorsCaspasesCyclosporineEnzyme InhibitorsEstradiolEstrogen Receptor alphaEstrogensFemaleIn Vitro TechniquesMiceMice, Inbred C57BLMice, KnockoutNeuronsPreoptic AreaCaspase InhibitorsCaspasesCyclosporineEnzyme InhibitorsEstradiolEstrogen Receptor alphaEstrogensTyrosine 3-Monooxygenase

Identifiers

PMID19657024
PMCPMC6428191
OpenAlexW2076975631

What OpenQuestion holds

Textmetadata
LicenceTDM
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.