Document Detail


Inhibitors of cysteine cathepsin and calpain do not prevent ultraviolet-B-induced apoptosis in human keratinocytes and HeLa cells.
MedLine Citation:
PMID:  15148608     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Caspases, members of the cysteine protease family, execute UVB-induced apoptosis in several cell lines and keratinocytes. Several researchers investigating UVB-induced apoptosis have demonstrated a dose-dependent protective effect of the synthetic peptide caspase inhibitor zVAD-fmk. However, zVAD-fmk displays a dose-dependent protective effect against UVB-induced apoptosis, even at doses higher than those required to block all known proapoptotic caspases. In addition, it is known that zVAD-fmk also inhibits other cysteine proteases including cathepsins and calpains, and these proteases have recently been demonstrated to play a role in the execution of programmed cell death induced by other stimuli, e.g. TNF-alpha. The purpose of the present study was therefore to investigate whether inhibitors of cysteine cathepsins and calpains could prevent UVB-induced apoptosis in HeLa cells and keratinocytes. This was done by investigating the effect of the irreversible cysteine protease inhibitor zFA-fmk, the cathepsin B inhibitor CA-074-Me and the calpain inhibitor ALLN on the viability of UVB-irradiated human keratinocytes and HeLa cells. At concentrations of 10 microM and above zVAD-fmk conferred partial dose-dependent protection against UVB-induced apoptosis in HeLa cells and keratinocytes. Moreover, caspase-3 activity was completely blocked at zVAD-fmk concentrations of 1 microM in HeLa cells. This indicates that caspase-independent mechanisms could be involved in UVB-induced apoptosis. However, the protease inhibitors zFA-fmk, CA-074-Me and ALLN all failed to prevent UVB-induced apoptosis in HeLa cells and keratinocytes. In conclusion, the protective effect of zVAD-fmk at high concentrations indicates that other proteases than caspases are active in the execution of UVB-induced apoptosis but further studies are needed to identify these proteases.
Authors:
Bo Bang; Ole Baadsgaard; Lone Skov; Marja Jäättelä
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-05-18
Journal Detail:
Title:  Archives of dermatological research     Volume:  296     ISSN:  0340-3696     ISO Abbreviation:  Arch. Dermatol. Res.     Publication Date:  2004 Jul 
Date Detail:
Created Date:  2004-07-27     Completed Date:  2005-01-31     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8000462     Medline TA:  Arch Dermatol Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  67-73     Citation Subset:  IM    
Copyright Information:
Copyright 2004 Springer-Verlag
Affiliation:
Department of Dermatology, Gentofte Hospital, Copenhagen, Denmark. bb22@bbh.hosp.dk
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Chloromethyl Ketones / pharmacology
Apoptosis / drug effects*,  physiology,  radiation effects
Calpain / antagonists & inhibitors
Caspases / antagonists & inhibitors
Cathepsins / antagonists & inhibitors
Cells, Cultured
Cysteine Proteinase Inhibitors / pharmacology*
Dipeptides / pharmacology
Hela Cells
Humans
Keratinocytes / cytology,  drug effects,  radiation effects
Ketones / pharmacology
Leupeptins / pharmacology
Phospholipases A / metabolism
Ultraviolet Rays
Chemical
Reg. No./Substance:
0/Amino Acid Chloromethyl Ketones; 0/CA 074 methyl ester; 0/Cysteine Proteinase Inhibitors; 0/Dipeptides; 0/Ketones; 0/Leupeptins; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 110044-82-1/acetylleucyl-leucyl-norleucinal; 96922-64-4/MDL 201053; EC 3.1.1.-/Phospholipases A; EC 3.4.-/Cathepsins; EC 3.4.22.-/Calpain; EC 3.4.22.-/Caspases

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