ID | 111524 |
著者 |
Takehara-Kasamatsu, Yuka
The University of Tokushima
Tsuchida, Kunihiro
The University of Tokushima|Fujita Health University
Nakatani, Masashi
The University of Tokushima|Fujita Health University
Murakami, Tatsuya
Fujita Health University
Kurisaki, Akira
The University of Tokushima
Hashimoto, Osamu
Kitasato University
Kurose, Hitomi
The University of Tokushima
Mori, Kazuhiro
The University of Tokushima
Sugino, Hiromu
The University of Tokushima
|
キーワード | FLRG
myostatin
activin
follistatin
heart
|
資料タイプ |
学術雑誌論文
|
抄録 | Follistatin-related gene (FLRG) encodes a secretory glycoprotein that has characteristic cysteine-rich follistatin domains. FLRG protein binds to and neutralizes several transforming growth factor-β (TGF-β) superfamily members, including myostatin (MSTN), which is a potent negative regulator of skeletal muscle mass. We have previously reported that FLRG was abundantly expressed in fetal and adult mouse heart. In this study, we analyzed the expression of FLRG mRNA during mouse heart development. FLRG mRNA was continuously expressed in the embryonic heart, whereas it was very low in skeletal muscles. By contrast, MSTN mRNA was highly expressed in embryonic skeletal muscles, whereas the expression of MSTN mRNA was rather low in the heart. In situ hybridization and immunohistochemical analysis revealed that FLRG expressed in smooth muscle of the aorta and pulmonary artery, valve leaflets of mitral and tricuspid valves, and cardiac muscles in the ventricle of mouse embryonic heart. However, MSTN was expressed in very limited areas, such as valve leaflets of pulmonary and aortic valves, the top of the ventricular and atrial septa. Interestingly, the expression of MSTN was complementary to that of FLRG, especially in the valvular apparatus. Biochemical analyses with surface plasmon resonance biosensor and reporter assays demonstrated that FLRG hardly dissociates from MSTN and activin once it bound to them, and efficiently inhibits these activities. Our results suggest that FLRG could function as a negative regulator of activin family members including MSTN during heart development.
|
掲載誌名 |
The Journal of Medical Investigation
|
ISSN | 13496867
13431420
|
cat書誌ID | AA11166929
AA12022913
|
出版者 | Faculty of Medicine Tokushima University
|
巻 | 54
|
号 | 3-4
|
開始ページ | 276
|
終了ページ | 288
|
並び順 | 276
|
発行日 | 2007-08
|
EDB ID | |
出版社版DOI | |
出版社版URL | |
フルテキストファイル | |
言語 |
eng
|
著者版フラグ |
出版社版
|
部局 |
医学系
生物資源系
|