Catechins activate muscle stem cells by Myf5 induction and stimulate muscle regeneration

Kim, A. Rum; Kim, Kyung Min; Byun, Mi Ran; Hwang, Jae Ho; Park, Jung Il; Oh, Ho Taek; Kim, Hyo Kyeong; Jeong, Mi Gyeong; Hwang, Eun Sook; Hong, Jeong Ho

doi:10.1016/j.bbrc.2017.05.114

Cited by 40 publications

(36 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Epigallocatechin gallate may also decrease the protein degradation rate caused by muscle atrophy, increase the expression of anabolic factors and promote the cross-sectional area of muscle fiber (Mirza et al 2014; Meador et al 2015). Catechins were also shown to promote the differentiation of myoblasts (Kim et al 2017). It is necessary to mention that the changes triggered by catechins involve the same pathways that we previously described to be engaged in vitamin D action in skeletal muscle.…”

Section: Vdr In Musculoskeletal Systemmentioning

confidence: 99%

Mechanisms of vitamin D on skeletal muscle function: oxidative stress, energy metabolism and anabolic state

2019

View full text Add to dashboard Cite

PurposeThis review provides a current perspective on the mechanism of vitamin D on skeletal muscle function with the emphasis on oxidative stress, muscle anabolic state and muscle energy metabolism. It focuses on several aspects related to cellular and molecular physiology such as VDR as the trigger point of vitamin D action, oxidative stress as a consequence of vitamin D deficiency.MethodThe interaction between vitamin D deficiency and mitochondrial function as well as skeletal muscle atrophy signalling pathways have been studied and clarified in the last years. To the best of our knowledge, we summarize key knowledge and knowledge gaps regarding the mechanism(s) of action of vitamin D in skeletal muscle.ResultVitamin D deficiency is associated with oxidative stress in skeletal muscle that influences the mitochondrial function and affects the development of skeletal muscle atrophy. Namely, vitamin D deficiency decreases oxygen consumption rate and induces disruption of mitochondrial function. These deleterious consequences on muscle may be associated through the vitamin D receptor (VDR) action. Moreover, vitamin D deficiency may contribute to the development of muscle atrophy. The possible signalling pathway triggering the expression of Atrogin-1 involves Src-ERK1/2-Akt- FOXO causing protein degradation.ConclusionBased on the current knowledge we propose that vitamin D deficiency results from the loss of VDR function and it could be partly responsible for the development of neurodegenerative diseases in human beings.

show abstract

Section: Vdr In Musculoskeletal Systemmentioning

confidence: 99%

Mechanisms of vitamin D on skeletal muscle function: oxidative stress, energy metabolism and anabolic state

2019

View full text Add to dashboard Cite

show abstract

“…Therefore, increasing the Myf5 positive satellite cell pool is a plausible strategy to enhance muscle regenerative capacity and combat some degenerative diseases caused by physiological aging or muscular dystrophies. For example, catechin has been reported to activate satellite cells by induction of Myf5 transcription and stimulate muscle regeneration ( Kim et al, 2017 ). In our study, for the first time, we detected the effect of salidroside on Myf5 expression and the number of Myf5 positive cells after terminal differentiation.…”

Section: Discussionmentioning

confidence: 99%

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

Zhang

Wang

et al. 2018

Front. Pharmacol.

View full text Add to dashboard Cite

Aim: Salidroside is an active compound extracted from Rhodiola rosea which 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.

show abstract

“…To identify the changes in the expression of the muscle differentiation-related genes induced by tannase-converted green tea extract administration, qRT-PCR was carried out and the results of the analysis are shown in Figure 4. Kim et al substantiated that catechins, such as ECG and EGCG, stimulate muscle regeneration by inducing the Myf5 transcription factor in the satellite cells [27]. Additionally, supplementation with EC appears to act as a muscle growth agent through modulation of myogenic conversion and differentiation-related promyogenic signaling factors [28].…”

Section: Evidence-based Complementary and Alternative Medicinementioning

confidence: 99%

Tannase‐Converted Green Tea Extract with High (−)‐Epicatechin Inhibits Skeletal Muscle Mass in Aged Mice

Hong

Lee

Kim³

et al. 2020

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

The objective of this study was to investigate the effects of tannase-converted green tea extract on body composition, muscle oxidative stress-related factors, and differentiation-related factors. The mean bone-related parameters and body composition were determined by the live dual-energy X-ray absorptiometry (DEXA). Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting were used to determine mRNA expression and protein levels, respectively. The results of total mass testing in the epicatechin control (EC) and middle concentration tannase-converted green tea extract (T1) intake groups were not significantly different compared with those in the control group; however, the high-concentration tannase-converted green tea extract (T2) group showed a significantly higher effect to the lean than that of all other groups (p<0.05). The results of the assay of muscle differentiation-related genes indicated that the expression levels in the EC and T1 groups (p<0.05) and the expression levels in the T2 group (p<0.01) were significantly different in the bicep femoris compared with that in the control group. The results of the SOD gene assay indicate that the expression levels in the EC and T1 groups (p<0.05) and the expression level in the T2 group (p<0.01) were significantly different in the bicep femoris compared with that in the control group. Additionally, SOD gene expression in the T2 group was significantly increased (p<0.05) in the soleus compared with that in the control, EC and T1 groups. Our results suggest that tannase-converted green tea extract prevents muscle loss and regulates the quantity and quality of muscle by the levels of antioxidant stress-related enzymes and muscle differentiation factors to a greater extent than the administration of epicatechin and middle dose green tea extract.

show abstract

Catechins activate muscle stem cells by Myf5 induction and stimulate muscle regeneration

Cited by 40 publications

References 22 publications

Mechanisms of vitamin D on skeletal muscle function: oxidative stress, energy metabolism and anabolic state

Mechanisms of vitamin D on skeletal muscle function: oxidative stress, energy metabolism and anabolic state

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

Tannase‐Converted Green Tea Extract with High (−)‐Epicatechin Inhibits Skeletal Muscle Mass in Aged Mice

Contact Info

Product

Resources

About