Evidence map›Paper›PMID 25344550›Full record

ArticleThe Journal of physiology2014

Role of cyclic AMP sensor Epac1 in masseter muscle hypertrophy and myosin heavy chain transition induced by β2-adrenoceptor stimulation.

Yoshiki Ohnuki, Daisuke Umeki, Yasumasa Mototani, Huiling Jin, Wenqian Cai, Kouichi Shiozawa, Kenji Suita, Yasutake Saeki, Takayuki Fujita, Yoshihiro Ishikawa and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. BetaThe Journal of physiology · 2018
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  15. Insulin/IGF1 signalling mediates the effects of βJournal of cachexia, sarcopenia and muscle · 2019
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  18. Epac activation inhibits IL-6-induced cardiac myocyte dysfunction.The journal of physiological sciences : JPS · 2018
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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

11 authors at 3 institutions in 1 country.

Yoshiki OhnukiDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Daisuke UmekiDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan Department of Orthodontics, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Yasumasa MototaniDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Huiling JinCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, 236-0004, Japan.
Wenqian CaiCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, 236-0004, Japan.
Kouichi ShiozawaDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Kenji SuitaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, 236-0004, Japan.
Yasutake SaekiDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan.
Takayuki FujitaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, 236-0004, Japan.
Yoshihiro IshikawaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, 236-0004, Japan.
Satoshi OkumuraDepartment of Physiology, Tsurumi University School of Dental Medicine, Yokohama, 230-8501, Japan Cardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, 236-0004, Japan okumura-s@tsurumi-u.ac.jp.
Tsurumi University · JPCardiovascular Institute Hospital · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The predominant isoform of β-adrenoceptor (β-AR) in skeletal muscle is β2-AR and that in the cardiac muscle is β1-AR. We have reported that Epac1 (exchange protein directly activated by cAMP 1), a new protein kinase A-independent cAMP sensor, does not affect cardiac hypertrophy in response to pressure overload or chronic isoproterenol (isoprenaline) infusion. However, the role of Epac1 in skeletal muscle hypertrophy remains poorly understood. We thus examined the effect of disruption of Epac1, the major Epac isoform in skeletal muscle, on masseter muscle hypertrophy induced by chronic β2-AR stimulation with clenbuterol (CB) in Epac1-null mice (Epac1KO). The masseter muscle weight/tibial length ratio was similar in wild-type (WT) and Epac1KO at baseline and was significantly increased in WT after CB infusion, but this increase was suppressed in Epac1KO. CB treatment significantly increased the proportion of myosin heavy chain (MHC) IIb at the expense of that of MHC IId/x in both WT and Epac1KO, indicating that Epac1 did not mediate the CB-induced MHC isoform transition towards the faster isoform. The mechanism of suppression of CB-mediated hypertrophy in Epac1KO is considered to involve decreased activation of Akt signalling. In addition, CB-induced histone deacetylase 4 (HDAC4) phosphorylation on serine 246 mediated by calmodulin kinase II (CaMKII), which plays a role in skeletal muscle hypertrophy, was suppressed in Epac1KO. Our findings suggest that Epac1 plays a role in β2-AR-mediated masseter muscle hypertrophy, probably through activation of both Akt signalling and CaMKII/HDAC4 signalling.

Indexed as

Adrenergic beta-2 Receptor AgonistsAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Guanine Nucleotide Exchange FactorsHistone DeacetylasesHypertrophyMasseter MuscleMiceMice, Inbred C57BLMice, Inbred CBAMyosin Heavy ChainsProtein IsoformsProto-Oncogene Proteins c-aktSignal TransductionAdrenergic beta-2 Receptor AgonistsCalcium-Calmodulin-Dependent Protein Kinase Type 2Epac protein, mouseGuanine Nucleotide Exchange FactorsHdac5 protein, mouseHistone DeacetylasesMyosin Heavy ChainsProtein IsoformsProto-Oncogene Proteins c-akt

Identifiers

PMID25344550
PMCPMC4270506
OpenAlexW2121270219

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.