Evidence map›Paper›PMID 25860951›Full record

ArticleInternational journal of molecular sciences2015

RNA sequencing identifies upregulated kyphoscoliosis peptidase and phosphatidic acid signaling pathways in muscle hypertrophy generated by transgenic expression of myostatin propeptide.

Yuanxin Miao, Jinzeng Yang, Zhong Xu, Lu Jing, Shuhong Zhao, Xinyun Li

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2015. 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
1.4field-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

14 citing papers in PubMed, 22 citations in OpenAlex.

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  9. The P2-receptor-mediated CaPurinergic signalling · 2019
    Article
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  11. Specific targeting of TGF-β family ligands demonstrates distinct roles in the regulation of muscle mass in health and disease.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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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

6 authors at 3 institutions in 2 countries.

Yuanxin MiaoKey Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China. miaoyuanxin19880610@126.com.
Jinzeng YangDepartment of Human Nutrition, Food and Animal Sciences, University of Hawaii at Manoa, Honolulu, HI 96822, USA. jinzeng@hawaii.edu.
Zhong XuKey Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China. xz8907@163.com.
Lu JingKey Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China. deer66@126.com.
Shuhong ZhaoKey Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China. shzhao@mail.hzau.edu.cn.
Xinyun LiKey Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China. xyli@mail.hzau.edu.cn.
Huazhong Agricultural University · CNCenter of Hubei Cooperative Innovation for Emissions Trading System · CNUniversity of Hawaiʻi at Mānoa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myostatin (MSTN), a member of the transforming growth factor-β superfamily, plays a crucial negative role in muscle growth. MSTN mutations or inhibitions can dramatically increase muscle mass in most mammal species. Previously, we generated a transgenic mouse model of muscle hypertrophy via the transgenic expression of the MSTN N-terminal propeptide cDNA under the control of the skeletal muscle-specific MLC1 promoter. Here, we compare the mRNA profiles between transgenic mice and wild-type littermate controls with a high-throughput RNA sequencing method. The results show that 132 genes were significantly differentially expressed between transgenic mice and wild-type control mice; 97 of these genes were up-regulated, and 35 genes were down-regulated in the skeletal muscle. Several genes that had not been reported to be involved in muscle hypertrophy were identified, including up-regulated myosin binding protein H (mybph), and zinc metallopeptidase STE24 (Zmpste24). In addition, kyphoscoliosis peptidase (Ky), which plays a vital role in muscle growth, was also up-regulated in the transgenic mice. Interestingly, a pathway analysis based on grouping the differentially expressed genes uncovered that cardiomyopathy-related pathways and phosphatidic acid (PA) pathways (Dgki, Dgkz, Plcd4) were up-regulated. Increased PA signaling may increase mTOR signaling, resulting in skeletal muscle growth. The findings of the RNA sequencing analysis help to understand the molecular mechanisms of muscle hypertrophy caused by MSTN inhibition.

Indexed as

AnimalsCytoskeletal ProteinsDown-RegulationHypertrophyMaleMembrane ProteinsMetalloendopeptidasesMiceMice, TransgenicMuscle ProteinsMuscle, SkeletalMuscular DiseasesMyostatinPeptide HydrolasesPhosphatidic AcidsRatsCytoskeletal ProteinsKY protein, mouseMembrane ProteinsMetalloendopeptidasesMuscle ProteinsMyostatinPeptide HydrolasesPhosphatidic AcidsRNA, MessengerZmpste24 protein, mouse

Identifiers

PMID25860951
PMCPMC4425062
OpenAlexW2047628240

What OpenQuestion holds

Textmetadata
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.