Evidence map›Paper›PMID 30819239›Full record

ArticleStem cell research & therapy2019

Continuous exposure of isoprenaline inhibits myoblast differentiation and fusion through PKA/ERK1/2-FOXO1 signaling pathway.

Shao-Juan Chen, Jing Yue, Jing-Xuan Zhang, Miao Jiang, Tu-Qiang Hu, Wei-Dong Leng, Li Xiang, Xin-Yuan Li, Lei Zhang, Fei Zheng and 7 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 31 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

17 authors at 2 institutions in 2 countries.

Shao-Juan ChenDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Jing YueDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Jing-Xuan ZhangDepartment of Physiology, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Miao JiangDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Tu-Qiang HuDepartment of Stomatology, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Wei-Dong LengDepartment of Stomatology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Li XiangDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Xin-Yuan LiDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Lei ZhangDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Fei ZhengDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Ye YuanDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Lin-Yun GuoDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Ya-Mu PanDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Yu-Wen YanDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Jia-Ning WangDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China.
Shi-You ChenDepartment of Physiology & Pharmacology, The University of Georgia, Athens, GA30602, USA.
Jun-Ming TangDepartment of Cardiology, and Institute of Clinical Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, People's Republic of China. tangjm416@163.com.
Hubei University of Medicine · CNTaihe Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThe objective of this study is to determine if exuberant sympathetic nerve activity is involved in muscle satellite cell differentiation and myoblast fusion. METHODS AND

resultsBy using immunoassaying and western blot analyses, we found that β1 and β2-adrenergic receptors (AdR) were expressed in C2C12 cells. The differentiated satellite cells exhibited an increased expression of β2-AdR, as compared with the proliferating cells. Continuous exposure of isoprenaline (ISO), a β-AdR agonist, delayed C2C12 cell differentiation, and myoblast fusion in time- and dose-dependent manner. ISO also increased short myotube numbers while decreasing long myotube numbers, consistent with the greater reduction in MyHC1, MyHC2a, and MyHC2x expression. Moreover, continuous exposure of ISO gradually decreased the ratio of PKA RI/RII, and PKA RI activator efficiently reversed the ISO effect on C2C12 cell differentiation and myoblast fusion while PKA inhibitor H-89 deteriorated the effects. Continuous single-dose ISO increased β1-AdR expression in C2C12 cells. More importantly, the cells showed enhanced phospho-ERK1/2 levels, resulting in increasing phospho-β2-AdR levels while decreasing β2-AdR levels, and the specific effects could be abolished by ERK1/2 inhibitor. Furthermore, continuous exposure of ISO induced FOXO1 nuclear translocation and increased the levels of FOXO1 in nuclear extracts while reducing pAKT, p-p38MAPK, and pFOXO1 levels. Conversely, blockade of ERK1/2 signaling partially abrogated ISO effects on AKT, p38MAPK, and FOXO1signaling, which partially restored C2C12 cell differentiation and myoblast fusion, leading to an increase in the numbers of medium myotube along with the increased expression of MyHC1 and MyHC2a.

conclusionContinuous exposure of ISO impedes satellite cell differentiation and myoblast fusion, at least in part, through PKA-ERK1/2-FOXO1 signaling pathways, which were associated with the reduced β2-AdR and increased β1-AdR levels.

Indexed as

Adrenergic beta-1 Receptor AgonistsAnimalsCell DifferentiationCell FusionCell ProliferationCyclic AMP-Dependent Protein KinasesForkhead Box Protein O1Gene Expression Regulation, DevelopmentalIsoproterenolMAP Kinase Signaling SystemMiceMuscle DevelopmentMyoblastsMyosin Heavy ChainsReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2Adrenergic beta-1 Receptor AgonistsCyclic AMP-Dependent Protein KinasesForkhead Box Protein O1Foxo1 protein, mouseIsoproterenolmyosin heavy chain-1, mouseMyosin Heavy ChainsReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2Adrenergic receptorDifferentiationERK1/2FOXO1IsoprenalineMyoblast fusionPKA

Identifiers

PMID30819239
PMCPMC6394105
OpenAlexW2915277235

What Socratic 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 Socratic graph.