Evidence map›Paper›PMID 28701790›Full record

ArticleScientific reports2017

Membrane progesterone receptor beta (mPRβ/Paqr8) promotes progesterone-dependent neurite outgrowth in PC12 neuronal cells via non-G protein-coupled receptor (GPCR) signaling.

Mayu Kasubuchi, Keita Watanabe, Kanako Hirano, Daisuke Inoue, Xuan Li, Kazuya Terasawa, Morichika Konishi, Nobuyuki Itoh, Ikuo Kimura

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.9field-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

28 citing papers in PubMed, 59 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

Mayu KasubuchiDepartment of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu-shi, Tokyo, 183-8509, Japan.
Keita WatanabeDepartment of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu-shi, Tokyo, 183-8509, Japan.
Kanako HiranoDepartment of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Science, Sakyo, Kyoto, 606-8501, Japan.
Daisuke InoueDepartment of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Science, Sakyo, Kyoto, 606-8501, Japan.
Xuan LiDepartment of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu-shi, Tokyo, 183-8509, Japan.
Kazuya TerasawaCenter for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Sakyo, Kyoto, 606-8501, Japan.
Morichika KonishiDepartment of Microbial Chemistry, Kobe Pharmaceutical University, Higashinada, Kobe, 658-8558, Japan.
Nobuyuki ItohDepartment of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Science, Sakyo, Kyoto, 606-8501, Japan.
Ikuo KimuraDepartment of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu-shi, Tokyo, 183-8509, Japan. ikimura@cc.tuat.ac.jp.
Tokyo University of Agriculture and Technology · JPKyoto University · JPKobe Pharmaceutical University · JPKyoto Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, sex steroid membrane receptors garnered world-wide attention because they may be related to sex hormone-mediated unknown rapid non-genomic action that cannot be currently explained by their genomic action via nuclear receptors. Progesterone affects cell proliferation and survival via non-genomic effects. In this process, membrane progesterone receptors (mPRα, mPRβ, mPRγ, mPRδ, and mPRε) were identified as putative G protein-coupled receptors (GPCRs) for progesterone. However, the structure, intracellular signaling, and physiological functions of these progesterone receptors are still unclear. Here, we identify a molecular mechanism by which progesterone promotes neurite outgrowth through mPRβ (Paqr8) activation. Mouse mPRβ mRNA was specifically expressed in the central nervous system. It has an incomplete GPCR topology, presenting 6 transmembrane domains and did not exhibit typical GPCR signaling. Progesterone-dependent neurite outgrowth was exhibited by the promotion of ERK phosphorylation via mPRβ, but not via other progesterone receptors such as progesterone membrane receptor 1 (PGRMC-1) and nuclear progesterone receptor in nerve growth factor-induced neuronal PC12 cells. These findings provide new insights of regarding the non-genomic action of progesterone in the central nervous system.

Indexed as

Neuronal OutgrowthAnimalsExtracellular Signal-Regulated MAP KinasesNerve Growth FactorNeuronsPC12 CellsPhosphatidylinositol 3-KinasesPhosphorylationProgesteroneRatsReceptors, G-Protein-CoupledReceptors, ProgesteroneSignal TransductionExtracellular Signal-Regulated MAP KinasesNerve Growth FactorPaqr8 protein, ratPhosphatidylinositol 3-KinasesProgesteroneprogesterone receptor BReceptors, G-Protein-CoupledReceptors, Progesterone

Identifiers

PMID28701790
PMCPMC5507890
OpenAlexW2725233258

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.