Evidence map›Paper›PMID 19340542›Full record

ArticleThe journal of physiological sciences : JPS2009

17beta-Estradiol-induced enhancement of estrogen receptor biosynthesis via MAPK pathway in mouse skeletal muscle myoblasts.

J Hatae, N Takami, Hai Lin, Akira Honda, R Inoue

Open access · goldAbstract read
In one paragraph

Article in The journal of physiological sciences : JPS, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  6. The Aqueous Extract ofAdvances in pharmacological and pharmaceutical sciences · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Epigenetics and breast cancers.Obstetrics and gynecology international · 2012
    Article
  12. Article
  13. Article
  14. Estrogen and its role in gastrointestinal health and disease.International journal of colorectal disease · 2009
    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

5 authors at 1 institution in 1 country.

J HataeDepartment of Physiology, School of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan. hatae@fukuoka-u.ac.jp
N Takami
Hai Lin
Akira Honda
R Inoue
Fukuoka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The skeletal muscle is one of the important target tissues for the actions of estrogen via both nuclear and extranuclear (non-genomic) pathways. However, there is a paucity of information about the receptor (ER) involved. The aim of this study was thus to explore the ER expression in skeletal muscle, and the influence of estrogen on it, by using C2C12 myoblasts derived from mouse skeletal muscle. Significant expression of a approximately 66-kD protein immunoreactive to ER type alpha (ERalpha) monoclonal antibody, which was comparable to that in ovary, was detected in the whole-cell (total) and nucleus-free (nonnuclear) fractions of C2C12 myoblasts. The expression level of these ER proteins increased in several hours with treatment with 17beta-estradiol (E2), which was preceded by the elevation of the ER mRNA level. This increase appeared to reflect the acceleration of de novo synthesis of ER protein, as proved by the (35)S-methionine immunoprecipitation method. A similar extent of fast increase in ER expression was also induced by a membrane-impermeable, BSA-conjugated estradiol (E2-BSA). Unexpectedly, the E2-induced increases in total and nonnuclear ER were further enhanced by the classic ER antagonists tamoxifen and ICI182,780 in a wide concentration range, implying some structural difference of the involved ER from the classical one. Treatment with the ERK1/2 inhibitor, PD98059 (10 microM), or the p38 MAPK-specific inhibitor, SB203580 (10 microM), greatly inhibited the E2-induced ER increase, while the protein kinase C (PKC) activator TPA (1 microM) enhanced it. These results collectively suggest that C2C12 skeletal myoblasts express a high level of ER, a considerable part of which is extranuclear. Further, the expression of ER in these cells may be significantly upregulated by estrogen itself via increased biosynthesis linked to membrane-bound ER and downstream MAPK-mediated signaling pathways.

Indexed as

AnimalsCell LineCell ProliferationDose-Response Relationship, DrugEnzyme InhibitorsEstradiolEstrogen AntagonistsEstrogensFlavonoidsFulvestrantImidazolesMiceMitogen-Activated Protein Kinase KinasesModels, AnimalMuscle, SkeletalMyoblasts, Skeletal2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneEnzyme InhibitorsEstradiolEstrogen AntagonistsEstrogensFlavonoidsFulvestrantImidazolesMitogen-Activated Protein Kinase KinasesPyridinesReceptors, EstrogenSB 203580Tamoxifen

Identifiers

PMID19340542
PMCPMC10717592
OpenAlexW2081875764

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.