Premium
Melatonin protects against apoptotic and autophagic cell death in C2C12 murine myoblast cells
Author(s) -
Kim Chi Hyun,
Kim Kyung Hwan,
Yoo YeongMin
Publication year - 2011
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2010.00833.x
Subject(s) - melatonin , programmed cell death , apoptosis , autophagy , biology , endocrinology , protein kinase b , medicine , c2c12 , wortmannin , microbiology and biotechnology , myocyte , biochemistry , myogenesis
In this study, we investigated whether or not melatonin inhibits apoptotic and autophagic cell death in C2C12 murine myoblast cells. Treatment of cells with S‐nitroso‐N‐acetylpenicillamine (SNAP), an NO donor, was shown to induce cell death, and treatment with melatonin (100 μ m ) significantly attenuated the occurrence of NO‐induced cell death. Decreased p‐Akt expression in response to NO was also arrested by melatonin. Under these conditions, p‐Bad (Ser 136) expression increased with melatonin treatment prior to NO treatment. Treatment with Akt inhibitors (LY 294002, wortmannin) plus melatonin reduced p‐Akt expression. Compared with NO treatment, Bcl‐2 expression increased with melatonin treatment, while Bax expression was inhibited by melatonin treatment. Expression of catalase and Mn‐superoxide dismutase (SOD) was elevated with melatonin treatment, whereas Cu/Zn‐SOD expression decreased with melatonin, lower than NO treatment, respectively. Next, we investigated the question of whether or not melatonin may restrain autophagic cell death in C2C12 cells. Nutrient starvation induced a rise in expression of the microtubule‐associated protein 1 light chain 3 (LC3)‐II; however, melatonin treatment suppressed LC3‐II expression by nutrient deprivation. Expression of Bcl‐2, Bax, catalase, and Cu/Zn‐SODs coincided with results of apoptotic cell death. Together, these results suggest that melatonin protects against apoptotic and autophagic cell death through the common pathway resulted in the increment of Bcl‐2 expression and the reduction of Bax expression in C2C12 murine myoblast cells.