scholarly journals Electroacupuncture suppresses myostatin gene expression: cell proliferative reaction in mouse skeletal muscle

2007 ◽  
Vol 30 (2) ◽  
pp. 102-110 ◽  
Author(s):  
Yutaka Takaoka ◽  
Mika Ohta ◽  
Akihiko Ito ◽  
Kunihiko Takamatsu ◽  
Aki Sugano ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cells ◽  
Expression Patterns ◽  
Low Frequency ◽  
Immunohistochemical Analysis ◽  
Long Term Effects ◽  
Transcription Control ◽  
Myostatin Gene ◽  
Mouse Skeletal Muscle

Complementary and alternative medicine (CAM) may provide patients with an alternative to traditional medicine, but an assessment of its efficacy is required. One CAM method, electroacupuncture (EA) treatment, is a maneuver that utilizes stimulation of acupuncture needles with a low-frequency microcurrent. To study the effect of short-term EA, we evaluated the differential expression of genes induced by EA in mouse skeletal muscle for up to 24 h. We then used RT-PCR to confirm the expression patterns of six differentially expressed genes. Bioinformatics analysis of their transcription control regions showed that EA-inducible genes have numerous common binding motifs that are related to cell differentiation, cell proliferation, muscle repair, and hyperplasia. These results suggested that EA treatment may induce cell proliferation in skeletal muscle. To verify this possibility, we used EA to stimulate mouse skeletal muscle daily for up to 1 mo and examined the long-term effects. Immunohistochemical analysis showed that nuclei of muscle cells treated with EA for 1 mo, especially nuclei of satellite cells, reacted with anti-human PCNA. Also, expression of the gene encoding myostatin, which is a growth repressor in muscle satellite cells, was suppressed by daily EA treatment for 1 wk; EA treatment for 1 mo resulted in more marked suppression of the gene. These molecular findings constitute strong evidence that EA treatment suppresses myostatin expression, which leads to a satellite cell-related proliferative reaction and repair in skeletal muscle.

Enhancement of Gene Delivery into Mouse Skeletal Muscle with Microbubble Destruction by Low-Frequency Ultrasound

2006 ◽  
Vol 36 (1) ◽  
pp. 32
Author(s):  
Sang Chol Lee ◽  
Sung Soo Jung ◽  
Seon Woon Kim ◽  
Sung Hoon Lim ◽  
Dae Kyung Cho ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Gene Delivery ◽  
Low Frequency ◽  
Mouse Skeletal Muscle ◽  
Low Frequency Ultrasound ◽  
Frequency Ultrasound

scholarly journals Akt1 deficiency diminishes skeletal muscle hypertrophy by reducing satellite cell proliferation

2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Protein Synthesis ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Mtor Signaling ◽  
Skeletal Muscle Hypertrophy ◽  
Satellite Cell Proliferation

Skeletal muscle mass is determined by the net dynamic balance between protein synthesis and degradation. Although the Akt/mechanistic target of rapamycin (mTOR)-dependent pathway plays an important role in promoting protein synthesis and subsequent skeletal muscle hypertrophy, the precise molecular regulation of mTOR activity by the upstream protein kinase Akt is largely unknown. In addition, the activation of satellite cells has been indicated as a key regulator of muscle mass. However, the requirement of satellite cells for load-induced skeletal muscle hypertrophy is still under intense debate. In this study, female germline Akt1 knockout (KO) mice were used to examine whether Akt1 deficiency attenuates load-induced skeletal muscle hypertrophy through suppressing mTOR-dependent signaling and satellite cell proliferation. Akt1 KO mice showed a blunted hypertrophic response of skeletal muscle, with a diminished rate of satellite cell proliferation following mechanical overload. In contrast, Akt1 deficiency did not affect the load-induced activation of mTOR signaling and the subsequent enhanced rate of protein synthesis in skeletal muscle. These observations suggest that the load-induced activation of mTOR signaling occurs independently of Akt1 regulation and that Akt1 plays a critical role in regulating satellite cell proliferation during load-induced muscle hypertrophy.

MiR-499/PRDM16 axis modulates the adipogenic differentiation of mouse skeletal muscle satellite cells

Human Cell ◽  
2018 ◽  
Vol 31 (4) ◽  
pp. 282-291 ◽  
Author(s):  
Juan Jiang ◽  
PengZhou Li ◽  
Hao Ling ◽  
ZhouZhou Xu ◽  
Bo Yi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Adipogenic Differentiation ◽  
Muscle Satellite Cells ◽  
Mouse Skeletal Muscle ◽  
Skeletal Muscle Satellite Cells

scholarly journals A Novel miRNA Y-56 Mediates The Proliferation of Porcine Skeletal Muscle Satellite Cells By Targeting IGF-1R

2021 ◽  
Author(s):  
Jie Song ◽  
Linlin Hao ◽  
Xiangfang Zeng ◽  
Rui Yang ◽  
Shiyan Qiao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Cyclin D1 ◽  
Satellite Cells ◽  
S Phase ◽  
Stem Cell Population ◽  
Muscle Satellite Cells ◽  
Expression Levels ◽  
Skeletal Muscle Satellite Cells ◽  
Novel Mirna

Abstract Background: The skeletal muscle phenotype of the Bama Xiang pig (BM) is significantly different from the Landrace pig (LP). Uncovering the mechanism of porcine skeletal muscle growth will be of great significance to elucidate the mechanism of the different formation. As the key post-transcriptional regulators, miRNAs play an indispensable role in skeletal muscle development. The proliferation of skeletal muscle satellite cells not only maintain the muscle stem cell population, but also provide a large number of muscle derived cells. Thus, the goal of this study is to explore the effects of a novel miRNA Y-56 on the porcine skeletal muscle satellite cells (PSCs). Results: Firstly, we found that Y-56 was highly expressed in porcine muscle tissues, and its expression was higher in the BM than the LP. The EdU staining and CCK-8 assays results showed that increased levels of Y-56 suppressed cell proliferation, whereas decreased levels of Y-56 resulted in the opposite consequences. Furthermore, flow cytometry results showed that overexpression of Y-56 significantly reduced the percentage of S-phase cells, and the qRT-PCR and western blotting results showed that the expression levels of cyclin dependent kinase 2 (CDK4), proliferating cell nuclear antigen (PCNA) and Cyclin D1 were significantly inhibited. Moreover, downregulation of Y-56 increased the number of S-phase cells and the expression of CDK, PCNA and Cyclin D1. Furtherly, we identified that insulin like growth factor-1 receptor (IGF-1R) was a direct target of Y-56. Consistently, overexpression of IGF-1R promoted the cell proliferation of the PSCs, and increased the number of S-phase cells, as well as up-regulated the expressions of CDK4, PCNA and Cyclin D1. Meanwhile, knock-down of IGF-1R was associated with the opposite tend. Finally, overexpression of IGF-1R partially reversed the inhibition of cell proliferation of the PSCs, the decrease of the percentage of S-phase cells and down-regulation of the expression levels of CDK4, PCNA and Cyclin D1, which caused by overexpression of Y-56. Conclusion: Collectively, our findings suggested that Y-56 represses proliferation and cell cycle process of the PSCs through several biological mechanisms involving downregulation of IGF-1R.

MiR-27b promotes sheep skeletal muscle satellite cell proliferation by targeting myostatin gene

2018 ◽  
Vol 97 (5) ◽  
pp. 1107-1117 ◽  
Author(s):  
Wei Zhang ◽  
Shi-Yin Wang ◽  
Shuang-Yi Deng ◽  
Li Gao ◽  
Li-Wei Yang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Muscle Satellite Cell ◽  
Myostatin Gene ◽  
Satellite Cell Proliferation ◽  
Skeletal Muscle Satellite Cell

Satellite cell proliferation and differentiation during postnatal growth of porcine skeletal muscle

2002 ◽  
Vol 282 (4) ◽  
pp. C899-C906 ◽  
Author(s):  
N. T Mesires ◽  
M. E. Doumit
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Nuclear Antigen ◽  
Positive Staining ◽  
Age Related ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Satellite Cell Proliferation

Age-related changes in satellite cell proliferation and differentiation during rapid growth of porcine skeletal muscle were examined. Satellite cells were isolated from hindlimb muscles of pigs at 1, 7, 14, and 21 wk of age (4 animals/age group). Satellite cells were separated from cellular debris by using Percoll gradient centrifugation and were adsorbed to glass coverslips for fluorescent immunostaining. Positive staining for neural cell adhesion molecule (NCAM) distinguished satellite cells from nonmyogenic cells. The proportion of NCAM-positive cells (satellite cells) in isolates decreased from 1 to 7 wk of age. Greater than 77% of NCAM-positive cells were proliferating cell nuclear antigen positive at all ages studied. Myogenin-positive satellite cells decreased from 30% at 1 wk to 14% at 7 wk of age and remained at constant levels thereafter. These data indicate that a high percentage of satellite cells remain proliferative during rapid postnatal muscle growth. The reduced proportion of myogenin-positive cells during growth may reflect a decrease in the proportion of differentiating satellite cells or accelerated incorporation of myogenin-positive cells into myofibers.

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