Document Detail


Binding of caspase-3 prodomain to heat shock protein 27 regulates monocyte apoptosis by inhibiting caspase-3 proteolytic activation.
MedLine Citation:
PMID:  17597071     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Caspase-3 is an essential executioner of apoptosis responsible for regulating many important cellular processes, among them the number of circulating monocytes, central players in the innate immune response. The activation of caspase-3 requires its processing from an inactive precursor. Here we show that the small heat shock protein 27 (Hsp27) associates with caspase-3 and protein-protein interaction experiments in vivo and with purified proteins demonstrate a direct interaction between Hsp27 and the amino-terminal prodomain of caspase-3. Using an in vitro caspase-3 activation assay, our results further establish that the interaction of Hsp27 with the caspase-3 prodomain inhibits the second proteolytic cleavage necessary for caspase-3 activation, revealing a novel mechanism for the regulation of this effector caspase. Hsp27 expression in monocytes is constitutive. Consistent with a central role of Hsp27 in blocking caspase-3 activation, Hsp27 down-regulation by double-stranded RNA interference induces apoptosis of macrophages, whereas Hsp27 overexpression increases the life span of monocytes by inhibiting apoptosis. Highlighting the importance of cell partitioning in the regulation of apoptosis, immunofluorescence, and subcellular fractionation studies revealed that whereas both caspase-3 and Hsp27 are cytoplasmic in fresh monocytes (i.e. not undergoing apoptosis), Hsp27 moves to the nucleus during apoptosis, a relocalization that can be blocked by promoting the differentiation of monocytes to macrophages or by inhibiting cell death. These results reveal a novel mechanism of caspase-3 regulation and underscore a novel and fundamental role of Hsp27 in the regulation of monocyte life span.
Authors:
Oliver H Voss; Sanjay Batra; Sunny J Kolattukudy; M Elba Gonzalez-Mejia; Jeffrey B Smith; Andrea I Doseff
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2007-06-27
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  282     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2007 Aug 
Date Detail:
Created Date:  2007-08-20     Completed Date:  2007-10-11     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  25088-99     Citation Subset:  IM    
Affiliation:
Heart and Lung Research Institute, Division of Pulmonary and Critical Care and Department of Molecular Genetics, The Ohio State University, Columbus, Ohio 43210, USA.
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MeSH Terms
Descriptor/Qualifier:
Antigens, CD14 / biosynthesis
Apoptosis
Caspase 3 / metabolism*
Cell Differentiation
Enzyme Activation
Enzyme Inhibitors / pharmacology*
Heat-Shock Proteins / metabolism*
Humans
Models, Biological
Monocytes / metabolism,  pathology*
Protein Binding
Protein Structure, Tertiary
RNA Interference
Subcellular Fractions / metabolism
Grant Support
ID/Acronym/Agency:
R01HL075040/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD14; 0/Enzyme Inhibitors; 0/Heat-Shock Proteins; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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