Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/14278
ชื่อเรื่อง: Calpastatin reduces calpain and caspase activation in methamphetamine-induced toxicity in human neuroblastoma SH-SY5Y cultured cells
ผู้แต่ง: Suwanjang W.
Phansuwan-Pujito P.
Govitrapong P.
Chetsawang B.
Keywords: calpain
calpastatin
caspase 3
methamphetamine
tyrosine 3 monooxygenase
article
cell culture
cell strain
cell viability
controlled study
enzyme activation
human
human cell
neuroblastoma
priority journal
protein blood level
protein degradation
protein phosphorylation
Calcium-Binding Proteins
Calpain
Caspase 3
Caspases
Cell Line, Tumor
Cell Survival
Central Nervous System Stimulants
Enzyme Activation
Humans
Methamphetamine
Neuroblastoma
Neuroprotective Agents
Phosphorylation
Tyrosine 3-Monooxygenase
วันที่เผยแพร่: 2012
บทคัดย่อ: Methamphetamine (METH) is an abused psychostimulant drug that can cause neurotoxicity to dopaminergic cells. It has been demonstrated that METH can induce caspase- and calpain-dependent death cascades. The purpose of the present study was to investigate the functional role of calpastatin, a specific endogenous calpain inhibitor protein, on caspase and calpain activation in METH-induced degeneration in neuroblastoma SH-SY5Y cell cultures. In this study, we found that METH significantly decreased cell viability, tyrosine hydroxylase phosphorylation and calpastatin levels. Supplementation of cells with exogenous calpastatin was able to reverse the toxic effect of METH on reduction in cell viability and tyrosine hydroxylase phosphorylation. METH also significantly increased calpain levels, the formation of calpain-specific breakdown products and cleaved caspase-3 levels; once again, these effects were diminished by pretreating the cells with calpastatin. These data suggest the contribution of calpastatin as a potential regulatory factor for calpain- and caspase-dependent death processes. © 2012 Elsevier Ireland Ltd.
URI: https://ir.swu.ac.th/jspui/handle/123456789/14278
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84865627845&doi=10.1016%2fj.neulet.2012.07.066&partnerID=40&md5=2d8a2ef1d039cfb3a49a19d8adc1634a
ISSN: 3043940
Appears in Collections:Scopus 1983-2021

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