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Salidroside Inhibits Myogenesis by Modulating p-Smad3-Induced Myf5 Transcription

Overview of attention for article published in Frontiers in Pharmacology, March 2018
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Title
Salidroside Inhibits Myogenesis by Modulating p-Smad3-Induced Myf5 Transcription
Published in
Frontiers in Pharmacology, March 2018
DOI 10.3389/fphar.2018.00209
Pubmed ID
Authors

Peng Zhang, Wenjiong Li, Lu Wang, Hongju Liu, Jing Gong, Fei Wang, Xiaoping Chen

Abstract

Aim: Salidroside is an active compound extracted fromRhodiola roseawhich is used to alleviate fatigue and enhance endurance in high altitude regions. Some studies have demonstrated that salidroside can affect precursor cell differentiation in hematopoietic stem cells, erythrocytes, and osteoblasts. The aim of this study was to investigate the effect of salidroside on myoblast differentiation and to explore the underlying molecular mechanisms of this effect.Methods:C2C12 myoblast cells were treated with different concentrations of salidroside in differentiation media. Real-time PCR, Western blotting, and immunofluorescence assay were employed to evaluate the effects of salidroside on C2C12 differentiation. RNA interference was used to reveal the important role of Myf5 in myogenesis inhibited by salidroside. Chromatin Immunoprecipitation and dual-luciferase reporter assay were utilized to explore the underlying mechanisms of salidroside-induced upregulation of Myf5.Results:We found that salidroside inhibits myogenesis by downregulating MyoD and myogenin, preserves undifferentiated reserve cell pools by upregulating Myf5. Knocking down Myf5 expression significantly rescued the myogenesis inhibited by salidroside. The effect of salidroside on myogenesis was associated with increased phosphorylated Smad3 (p-Smad3). Both SIS3 (Specific inhibitor of p-Smad3) and dominant negative Smad3 plasmid (DN-Smad3) attenuated the inhibitory effect of salidroside on C2C12 differentiation. Moreover, the induction of Myf5 transcription by salidroside was dependent on a Smad-binding site in the promoter region of Myf5 gene.Conclusion and Implications:Our findings identify a novel role and mechanism for salidroside in regulating myogenesis through p-Smad3-induced Myf5 transcription, which may have implications for its further application in combating degenerative muscular diseases caused by depletion of muscle stem cells, such as Duchenne muscular dystrophy or sarcopenia.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 33 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 33 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 21%
Student > Ph. D. Student 4 12%
Student > Master 3 9%
Student > Bachelor 2 6%
Other 2 6%
Other 1 3%
Unknown 14 42%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 5 15%
Biochemistry, Genetics and Molecular Biology 5 15%
Medicine and Dentistry 3 9%
Psychology 2 6%
Agricultural and Biological Sciences 1 3%
Other 2 6%
Unknown 15 45%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 30 March 2018.
All research outputs
#17,933,348
of 23,026,672 outputs
Outputs from Frontiers in Pharmacology
#7,213
of 16,337 outputs
Outputs of similar age
#241,963
of 332,696 outputs
Outputs of similar age from Frontiers in Pharmacology
#171
of 377 outputs
Altmetric has tracked 23,026,672 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 16,337 research outputs from this source. They receive a mean Attention Score of 5.0. This one is in the 48th percentile – i.e., 48% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 332,696 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 22nd percentile – i.e., 22% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 377 others from the same source and published within six weeks on either side of this one. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.