Identification and Characterization of Follistatin-Related Protein-1 Involved in the Regulation of Chinese Perch Skeletal Muscle Hyperplasia

被引:8
作者
Chu, W. [1 ,2 ]
Cheng, J. [1 ]
Zhu, X. [1 ]
Wu, P. [1 ]
Chen, L. [1 ]
Wang, J. [1 ]
Wu, Y. [3 ]
Zeng, M. [3 ]
Zhang, J. [1 ,2 ]
机构
[1] Changsha Univ, Dept Bioengn & Environm Sci, Changsha 410003, Hunan, Peoples R China
[2] Collaborat Innovat Ctr Efficient & Hlth Prod Fish, Changde 415000, Peoples R China
[3] Inst Hunan Aquaculture & Fishes, Changsha, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
Siniperca chuatsi; follistatin-related protein; myostatin; satellite cell; muscle growth; hyperplasia; SATELLITE CELL; GENE; MYOSTATIN; EXPRESSION; BINDING; CLONING; INDUCTION; ACTIVIN; TARGET; PAX7;
D O I
10.2174/1566524016666160607122105
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Follistatin-related protein (FSRP), which belongs to a member of the follistatin family, has been postulated to be a new negative regulator of myostatin (MSTN) and is involved in muscle development. In this study, we cloned the complete cDNA sequence of FSRP-1 from Chinese perch muscle. FSRP-1 mRNA was highly expressed in the fast muscle and brain tissue of adult fish. The expression of FSRP-1 rapidly increased at 90 days post hatching (dph) in the fast muscle of Chinese perch. Furthermore, to investigate the roles of FSRP-1 in muscle growth, we constructed a FSRP-1 expression vector and isolated FSRP-1 fusion protein. The purified FSRP-1 fusion protein was injected into the muscle tissues of the Chinese perch (90 dph). The results showed that the number of muscle fibers and the satellite cell activation frequency were increased in the FSRP-1 treatment group. In addition, the myostatin (MSTN) expression was significantly decreased upon the FSRP-1 treatment. Collectively, the results suggest a possible mechanism of the FSRP-1 for inhibiting MSTN activity and enhancing muscle growth and renewal in vivo, and it may provide an applicable implication for the defected muscle repairing and regeneration.
引用
收藏
页码:596 / 604
页数:9
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