The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiation

被引：0
作者：
W Luo
H Wu
Y Ye
Z Li
S Hao
L Kong
X Zheng
S Lin
Q Nie
X Zhang
机构：
[1] Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding,Department of Animal Genetics
[2] and Key Lab of Chicken Genetics,Department of Veterinary Biomedicine
[3] Breeding and Reproduction,Department of Animal Science
[4] Ministry of Agriculture,undefined
[5] South China Agricultural University,undefined
[6] Guangzhou,undefined
[7] Breeding and Reproduction,undefined
[8] College of Animal Science,undefined
[9] South China Agricultural University,undefined
[10] Guangzhou,undefined
[11] College of Veterinary Medicine,undefined
[12] South China Agricultural University,undefined
[13] Guangzhou,undefined
[14] College of Life Science,undefined
[15] Foshan University,undefined
[16] Foshan,undefined
来源：
Cell Death & Disease | 2014年 / 5卷
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摘要：
Previous studies have shown that miR-203 is a skin-specific microRNA (miRNA) with a profound role in skin cell differentiation. However, emerging microarray and deep sequencing data revealed that miR-203 is also expressed in embryonic skeletal muscle and myoblasts. In this study, we found that miR-203 was transiently upregulated in chicken embryos on days 10 to 16 (E10–E16) and was sharply downregulated and even not expressed after E16 in chicken embryonic skeletal muscle. Histological profiles and weight variations of embryo skeletal muscle revealed that miR-203 expression is correlated with muscle development. In vitro experiments showed that miR-203 exhibited downregulated expression during myoblast differentiation into myotubes. miR-203 overexpression inhibited myoblast proliferation and differentiation, whereas its loss-of-function increased myoblast proliferation and differentiation. During myogenesis, miR-203 can target and inhibit the expression of c-JUN and MEF2C, which were important for cell proliferation and muscle development, respectively. The overexpression of c-JUN significantly promoted myoblast proliferation. Conversely, knockdown of c-JUN by siRNA suppressed myoblast proliferation. In addition, the knockdown of MEF2C by siRNA significantly inhibited myoblast differentiation. Altogether, these data not only suggested that the expression of miR-203 is transitory during chicken skeletal muscle development but also showed a novel role of miR-203 in inhibiting skeletal muscle cell proliferation and differentiation by repressing c-JUN and MEF2C, respectively.
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页码：e1347 / e1347
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共 266 条
[1]  
Perry RL(2000)Molecular mechanisms regulating myogenic determination and differentiation Front Biosci 5 D750-D767
[2]  
Rudnick MA(2011)IGF-II is regulated by microRNA-125b in skeletal myogenesis J Cell Biol 192 69-81
[3]  
Ge Y(1999)MEF2: a transcriptional target for signaling pathways controlling skeletal muscle growth and differentiation Curr Opin Cell Biol 11 683-688
[4]  
Sun Y(2011)Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis Nat Rev Mol Cell Biol 12 349-361
[5]  
Chen J(2001)Skeletal muscle formation in vertebrates Curr Opin Genet Dev 11 440-448
[6]  
Naya FJ(2012)Myoblast fusion: lessons from flies and mice Development 139 641-656
[7]  
Olson E(2012)Satellite cells are essential for skeletal muscle regeneration: the cell on the edge returns centre stage Development 139 2845-2856
[8]  
Braun T(1998)Transcriptional control of muscle development by myocyte enhancer factor-2 (MEF2) proteins Annu Rev Cell Dev Biol 14 167-196
[9]  
Gautel M(1995)A series of mutations in the D-MEF2 transcription factor reveal multiple functions in larval and adult myogenesis in Dev Biol 171 169-181
[10]  
Buckingham M(1995)Requirement of MADS domain transcription factor D-MEF2 for muscle formation in Science 267 688-693
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