Shinichiro Nishimatsu
Department Kawasaki Medical School Kawasaki Medical School, Department of Natural Sciences, Position Professor |
|
Article types | 原著 |
Language | English |
Peer review | Peer reviewed |
Title | A missense mutant myostatin causes hyperplasia without hypertrophy in the mouse muscle. |
Journal | Formal name:Biochemical and biophysical research communications Abbreviation:Biochem Biophys Res Commun ISSN code:0006291X/10902104 |
Volume, Issue, Page | 293(1),pp.247-251 |
Author and coauthor | Nishi Masumi, Yasue Akihiro, Nishimatu Shinichirou, Nohno Tsutomu, Yamaoka Takashi, Itakura Mitsuo, Moriyama Keiji, Ohuchi Hideyo, Noji Sumihare |
Publication date | 2002/04 |
Summary | Myostatin, which is a member of the TGF-beta superfamily, is a negative regulator of skeletal muscle formation. Double-muscled Piedmontese cattle have a C313Y mutation in myostatin and show increased skeletal muscle mass which resulted from an increase of myofiber number (hyperplasia) without that of myofiber size (hypertrophy). To examine whether this mutation in myostatin gene affects muscle development in a dominant negative manner, we generated transgenic mice overexpressing the mutated gene. The transgenic mice exhibited dramatic increases in the skeletal muscle mass resulting from hyperplasia without hypertrophy. In contrast, it has been reported that a myostatin mutated at its cleavage site produces hypertrophy without hyperplasia in the muscle. Thus, these results suggest that (1) the myostatin containing the missense mutation exhibits a dominant negative activity and that (2) there are two types in the dominant negative form of myostatin, causing either hypertrophy or hyperplasia. |
DOI | 10.1016/S0006-291X(02)00209-7 |
Document No. | 12054591 |