Premium
Calpeptin attenuated apoptosis and intracellular inflammatory changes in muscle cells
Author(s) -
Nozaki Kenkichi,
Das Arabinda,
Ray Swapan K.,
Banik Naren L.
Publication year - 2011
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22585
Subject(s) - calpain , inflammation , extracellular , intracellular , microbiology and biotechnology , tumor necrosis factor alpha , apoptosis , biology , chemistry , immunology , cancer research , biochemistry , enzyme
Abstract In idiopathic inflammatory myopathies (IIMs), extracellular inflammatory stimulation is considered to induce secondary intracellular inflammatory changes including expression of major histocompatibility complex class‐I (MHC‐I) and to produce a self‐sustaining loop of inflammation. We hypothesize that activation of calpain, a Ca 2+ ‐sensitive protease, bridges between these extracellular inflammatory stress and intracellular secondary inflammatory changes in muscle cells. In this study, we demonstrated that treatment of rat L6 myoblast cells with interferon‐γ (IFN‐γ) caused expression of MHC‐I and inflammation‐related transcription factors (phosphorylated‐extracellular signal‐regulated kinase 1/2 and nuclear factor‐κB). We also demonstrated that treatment with tumor necrosis factor‐α (TNF‐α) induced apoptotic changes and activation of calpain and cyclooxygenase‐2. Furthermore, we found that posttreatment with calpeptin attenuated the intracellular changes induced by IFN‐γ or TNF‐α. Our results indicate that calpain inhibition attenuates apoptosis and secondary inflammatory changes induced by extracellular inflammatory stimulation in the muscle cells. These results suggest calpain as a potential therapeutic target for treatment of IIMs. © 2011 Wiley‐Liss, Inc