Evidence map›Paper›PMID 26465008›Full record

ArticleeNeuro

Estradiol Preferentially Induces Progestin Receptor-A (PR-A) Over PR-B in Cells Expressing Nuclear Receptor Coactivators in the Female Mouse Hypothalamus

Kalpana D Acharya, Sarah D Finkelstein, Elizabeth P Bless, Sabin A Nettles, Biserka Mulac-Jericevic, Orla M Conneely, Shaila K Mani, Marc J Tetel

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
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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

8 authors at 2 institutions in 1 country.

Kalpana D AcharyaNeuroscience Program, Wellesley College , Wellesley, Massachusetts 02481.
Sarah D FinkelsteinNeuroscience Program, Wellesley College , Wellesley, Massachusetts 02481.
Elizabeth P BlessNeuroscience Program, Wellesley College , Wellesley, Massachusetts 02481.
Sabin A NettlesNeuroscience Program, Wellesley College , Wellesley, Massachusetts 02481.
Biserka Mulac-JericevicDepartment of Molecular and Cellular Biology, Baylor College of Medicine , Houston, Texas 77030.
Orla M ConneelyDepartment of Molecular and Cellular Biology, Baylor College of Medicine , Houston, Texas 77030.
Shaila K ManiDepartment of Molecular and Cellular Biology, Baylor College of Medicine , Houston, Texas 77030.
Marc J TetelNeuroscience Program, Wellesley College , Wellesley, Massachusetts 02481.
Wellesley College · USBaylor College of Medicine · US

Funding

Mechanisms of Steroid Hormone Action in BrainR01DK061935 · NIDDK · WELLESLEY COLLEGE · PI TETEL, MARC JEFFREY · 2002 to 2014
$2.7M
NIDDK NIH HHS R01 DK061935
6 · The paper itself

Abstract

Estrogens act in brain to profoundly influence neurogenesis, sexual differentiation, neuroprotection, cognition, energy homeostasis, and female reproductive behavior and physiology through a variety of mechanisms, including the induction of progestin receptors (PRs). PRs are expressed as two isoforms, PR-A and PR-B, that have distinct functions in physiology and behavior. Because these PR isoforms cannot be distinguished using cellular resolution techniques, the present study used isoform-specific null mutant mice that lack PR-A or PR-B for the first time to investigate whether 17β-estradiol benzoate (EB) regulates the differential expression of the PR isoforms in the ventromedial nucleus of the hypothalamus (VMN), arcuate nucleus, and medial preoptic area, brain regions that are rich in EB-induced PRs. Interestingly, EB induced more PR-A than PR-B in all three brain regions, suggesting that PR-A is the predominant isoform in these regions. Given that steroid receptor coactivator (SRC)-1 and SRC-2 are important in estrogen receptor (ER)-dependent transcription in brain, including PR induction, we tested whether the expression of these coactivators was correlated with PR isoform expression. The majority of EB-induced PR cells expressed both SRC-1 and SRC-2 in the three brain regions of all genotypes. Interestingly, the intensity of PR-A immunoreactivity correlated with SRC-2 expression in the VMN, providing a potential mechanism for selective ER-mediated transactivation of PR-A over PR-B in a brain region-specific manner. In summary, these novel findings indicate that estrogens differentially regulate PR-A and PR-B expression in the female hypothalamus, and provide a mechanism by which steroid action in brain can selectively modulate behavior and physiology.

Indexed as

estrogensfemale reproductionprogesteroneSRC-1steroid receptor coactivatorventromedial hypothalamus

Identifiers

PMID26465008
PMCPMC4596027
OpenAlexW2176004569

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.