Abstract：
:The mechanism of fibrate-induced myopathy was investigated in this report. When clofibrate (30 to 300 microM) was applied to L6 rat skeletal myoblasts, dose-dependently apoptosis was observed within 24 h. In the apoptotic myoblasts, a caspase-12 cleavage was observed at 2 h and with following caspases-9 and -3-related cascade activation. In contrast, the neutral protease calpain, that is a key enzyme in ER stress-related apoptosis via caspase-12 activation, was significantly decreased during apoptosis. Next, the authors evaluated a role of calcium-dependent signal(s). When clofibrate was added into medium, cytosolic calcium concentration was rapidly and persistently increased. On the other hand, an addition of 10 mM EGTA depressed sustained calcium phase, and concurrent myoblasts apoptosis was completely inhibited. Taken together, our findings indicate that the clofibrate-induced myopathy is triggered by Ca2+ influx, then activated cytosolic caspase-12 through calpain-independent cascade, and consequently caused apoptotic DNA fragmentation.
journal_name
Life Scijournal_title
Life sciencesauthors
Matzno S,Yasuda S,Kitada Y,Akiyoshi T,Tanaka N,Juman S,Shinozuka K,Nakabayashi T,Matsuyama Kdoi
10.1016/j.lfs.2005.08.003subject
Has Abstractpub_date
2006-03-13 00:00:00pages
1892-9issue
16eissn
0024-3205issn
1879-0631pii
S0024-3205(05)00914-8journal_volume
78pub_type
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