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Melatonin protects SH‐SY5Y neuroblastoma cells from calyculin A‐induced neurofilament impairment and neurotoxicity
Author(s) -
Li Shu Peng,
Deng Yan Qiu,
Wang Xiao Chuan,
Wang Yi Peng,
Wang JianZhi
Publication year - 2004
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.2004.00116.x
Subject(s) - hyperphosphorylation , viability assay , sh sy5y , melatonin , neurofilament , neurotoxicity , biology , microbiology and biotechnology , cytoskeleton , neuroblastoma , phosphorylation , cell , medicine , endocrinology , cell culture , toxicity , biochemistry , immunology , genetics , immunohistochemistry
Hyperphosphorylation of cytoskeletal proteins seen in Alzheimer's disease is most probably the result of an imbalanced regulation in protein kinases and protein phosphatases (PP) in the affected neurons. Previous studies have revealed that PP‐2A and PP‐1 play important roles in the pathogenesis. Employing human neuroblastoma cells, we found that 10 n m calyculin A (CA), a selective inhibitor of PP‐2A and PP‐1, significantly increased phosphorylation and accumulation of neurofilament (NF) in the cells. Levels of NF‐M (middle chain) and NF‐L (light chain) mRNA decreased after CA treatment. Additionally, CA led to a decreased cell viability determined by MTT and crystal violet assay. Melatonin efficiently protects the cell from CA‐induced alterations in NF hyperphosphorylation and accumulation, suppressed NF gene expression as well as decreased cell viability. It is concluded that inhibition of PP‐2A/PP‐1 by CA induces abnormalities in NF metabolism and cell survival, and melatonin efficiently arrests the lesions.