ABSTRACT
Extracellular ATP (exATP) has been known to be a critical ligand regulating skeletal muscle differentiation and contractibility. ExATP synthesis was greatly increased with the high level of adenylate kinase 1 (AK1) and ATP synthase beta during C2C12 myogenesis. The exATP synthesis was abolished by the knock-down of AK1 but not by that of ATP synthase beta in C2C12 myotubes, suggesting that AK1 is required for exATP synthesis in myotubes. However, membrane-bound AK1beta was not involved in exATP synthesis because its expression level was decreased during myogenesis in spite of its localization in the lipid rafts that contain various kinds of receptors and mediate cell signal transduction, cell migration, and differentiation. Interestingly, cytoplasmic AK1 was secreted from C2C12 myotubes but not from C2C12 myoblasts. Taken together all these data, we can conclude that AK1 secretion is required for the exATP generation in myotubes.
Subject(s)
Animals , Mice , Adenosine Triphosphate/biosynthesis , Adenylate Kinase/metabolism , Cell Line , Extracellular Space/metabolism , Isoenzymes/metabolism , Muscles/cytologyABSTRACT
Shenqi-wan, Oriental herbal medicine formulation, has been traditionally used for delayed mental and physical development in children, complications of diabetes, and glomerulonephritis. In the present study, the protective effect of the aqueous extract of Shenqi-wan against traumatic brain injury (TBI) in the rat hippocampal dentate gyrus was investigated. For this study, step-down avoidance task, terminal deoxynuclotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, Bax immunohistochemistry, and 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry were conducted. In the present results, it was shown that apoptotic cell death and cell proliferation in the dentate gyrus were significantly increased following TBI in rats and that the aqueous extract of Shenqi-wan suppressed the TBI-induced increase in apoptosis and cell proliferation in the dentate gyrus. Based on the present results, it is possible that the aqueous extract of Shenqi-wan has a neuroprotective effect on TBI-induced neuronal cell death.