| RRC ID |
54886
|
| 著者 |
Adachi N, Kanazawa I, Tanaka KI, Takeno A, Notsu M, Tanaka S, Sugimoto T.
|
| タイトル |
Insulin-Like Growth Factor-I Protects Against the Detrimental Effects of Advanced Glycation End Products and High Glucose in Myoblastic C2C12 Cells.
|
| ジャーナル |
Calcif Tissue Int
|
| Abstract |
Previous studies suggested that advanced glycation end products (AGEs) and insulin-like growth factor-I (IGF-I) are involved in the mechanism of diabetes-induced sarcopenia. In this study, we examined effects of treatments with AGEs and/or IGF-I for 24 h on myogenic differentiation and apoptosis in mouse myoblastic C2C12 cells. Real-time PCR and Western blot were performed to investigate mRNA and protein expressions, and apoptosis was examined by using a DNA fragment detection ELISA kit. AGE3 significantly decreased mRNA and protein expressions of MyoD and Myogenin, whereas IGF-I significantly increased them and attenuated the effects of AGE3. AGEs significantly decreased endogenous IGF-I mRNA expression and suppressed IGF-I-induced Akt activation. High glucose (22 mM) significantly increased mRNA expression of Rage, a receptor for AGEs, while IGF-I significantly decreased it. DNA fragment ELISA showed that AGE2 and AGE3 significantly increased apoptosis of C2C12 cells, whereas IGF-I significantly suppressed the AGE2- and AGE3-induced apoptosis. In contrast, high glucose enhanced AGE3-induced apoptosis. IGF-I significantly attenuated the effects of high glucose plus AGE3 on the mRNA and protein expressions of MyoD and Myogenin as well as the apoptosis. These findings indicate that AGEs inhibit myogenic differentiation and increase apoptosis in C2C12 cells, and that high glucose increases RAGE and enhances the AGE3-induced apoptosis, suggesting that AGEs and high glucose might contribute to the reduction of muscle mass and function. Moreover, IGF-I attenuated the detrimental effects of AGEs and high glucose in myoblastic cells; thus, IGF-I-Akt signal could be a therapeutic target of DM-induced sarcopenia.
|
| 巻・号 |
105(1)
|
| ページ |
89-96
|
| 公開日 |
2019-7-1
|
| DOI |
10.1007/s00223-019-00537-w
|
| PII |
10.1007/s00223-019-00537-w
|
| PMID |
30809689
|
| MeSH |
Animals
Apoptosis / drug effects
Cell Differentiation / drug effects
Cell Differentiation / physiology
Cell Line
Glucose / metabolism
Glycation End Products, Advanced / drug effects*
Glycation End Products, Advanced / metabolism
Insulin-Like Growth Factor I / metabolism
Insulin-Like Growth Factor I / pharmacology*
Mice
Myoblasts / drug effects*
Myoblasts / metabolism
Osteoblasts / drug effects*
Osteoblasts / metabolism
|
| IF |
3.265
|
| 引用数 |
2
|
| リソース情報 |
| ヒト・動物細胞 |
C2C12(RCB0987) |
