Document Detail


Upregulation and activation of caspase-3 or caspase-8 and elevation of intracellular free calcium mediated apoptosis of indomethacin-induced K562 cells.
MedLine Citation:
PMID:  15265368     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: A nonsteroidal anti-inflammatory drug, indomethacin, has been shown to have anti-leukemic activity and induce leukemic cell apoptosis. This study was to elucidate the mechanism of indomethacin-induced K562 cell apoptosis. METHODS: K562 cells were grown in RPMI 1640 medium and treated with different doses of indomethacin (0 micromol/L, 100 micromol/L, 200 micromol/L, 400 micromol/L, 800 micromol/L) for 72 hours. The cells were harvested, and cell viability or apoptosis was analyzed using MTT assay and AO/EB stain, combining laser scanning confocal microscopy (LSCM) technique separately. For the localization and distribution of intracellular caspase-3 or caspase-8 protein, immunofluorescence assay was carried out. To reveal the activation of caspase-3 or caspase-8 in indomethacin-treated cells, Western blot detection was used. The change in intracellular free calcium was determined by Fluo-3/Am probe labeling combined with LSCM. RESULTS: Indomethacin could lead to K562 cell apoptosis and inhibit cell viability in a concentration-dependent manner. An increased expression of intracellular caspase-3 or caspase-8 was observed at higher doses of indomethacin (400 - 800 micromol/L). Western blot results showed upregulation and activation in both caspase-3 and caspase-8 protein. Under indomethacin intervention, the levels of intracellular free calcium showed a significant increase. Blocking the activity of cyclooxygenase did not abolish the effects of indomethacin on K562 cell apoptosis. CONCLUSIONS: Activation and upregulation of caspase-3 or caspase-8 protein were responsible for Indomethacin-induced K562 cell apoptosis. Variation of intracellular free calcium might switch on the apoptotic pathway and the proapoptotic effect of indomethacin might be cyclooxygenase-independent.
Authors:
Guang-sen Zhang; Guang-biao Zhou; Chong-wen Dai
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Chinese medical journal     Volume:  117     ISSN:  0366-6999     ISO Abbreviation:  Chin. Med. J.     Publication Date:  2004 Jul 
Date Detail:
Created Date:  2004-07-21     Completed Date:  2004-10-28     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7513795     Medline TA:  Chin Med J (Engl)     Country:  China    
Other Details:
Languages:  eng     Pagination:  978-84     Citation Subset:  IM    
Affiliation:
Institute of Molecular Hematology/Division of Hematology, Second Xiang-Ya Hospital, Central South University, Changsha, Hunan 410011, China. zgsllzy@public.cs.hn.cn
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Calcium / metabolism*
Caspase 3
Caspase 8
Caspases / genetics*,  metabolism
Cyclooxygenase Inhibitors / pharmacology
Enzyme Activation
Gene Expression Regulation, Enzymologic / drug effects*
Humans
Indomethacin / pharmacology*
K562 Cells
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 53-86-1/Indomethacin; 7440-70-2/Calcium; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP8 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspases

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