Document Detail


Polymerization of MIP-1 chemokine (CCL3 and CCL4) and clearance of MIP-1 by insulin-degrading enzyme.
MedLine Citation:
PMID:  20959807     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Macrophage inflammatory protein-1 (MIP-1), MIP-1α (CCL3) and MIP-1β (CCL4) are chemokines crucial for immune responses towards infection and inflammation. Both MIP-1α and MIP-1β form high-molecular-weight aggregates. Our crystal structures reveal that MIP-1 aggregation is a polymerization process and human MIP-1α and MIP-1β form rod-shaped, double-helical polymers. Biophysical analyses and mathematical modelling show that MIP-1 reversibly forms a polydisperse distribution of rod-shaped polymers in solution. Polymerization buries receptor-binding sites of MIP-1α, thus depolymerization mutations enhance MIP-1α to arrest monocytes onto activated human endothelium. However, same depolymerization mutations render MIP-1α ineffective in mouse peritoneal cell recruitment. Mathematical modelling reveals that, for a long-range chemotaxis of MIP-1, polymerization could protect MIP-1 from proteases that selectively degrade monomeric MIP-1. Insulin-degrading enzyme (IDE) is identified as such a protease and decreased expression of IDE leads to elevated MIP-1 levels in microglial cells. Our structural and proteomic studies offer a molecular basis for selective degradation of MIP-1. The regulated MIP-1 polymerization and selective inactivation of MIP-1 monomers by IDE could aid in controlling the MIP-1 chemotactic gradient for immune surveillance.
Authors:
Min Ren; Qing Guo; Liang Guo; Martin Lenz; Feng Qian; Rory R Koenen; Hua Xu; Alexander B Schilling; Christian Weber; Richard D Ye; Aaron R Dinner; Wei-Jen Tang
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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:  2010-10-19
Journal Detail:
Title:  The EMBO journal     Volume:  29     ISSN:  1460-2075     ISO Abbreviation:  EMBO J.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-02     Completed Date:  2011-01-12     Revised Date:  2011-12-21    
Medline Journal Info:
Nlm Unique ID:  8208664     Medline TA:  EMBO J     Country:  England    
Other Details:
Languages:  eng     Pagination:  3952-66     Citation Subset:  IM    
Affiliation:
Ben-May Department for Cancer Research, The University of Chicago, Chicago, IL 60637, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Cell Line
Chemokine CCL3 / chemistry*,  genetics,  immunology,  metabolism*
Chemokine CCL4 / chemistry*,  genetics,  immunology,  metabolism*
Crystallography, X-Ray
Humans
Insulysin / chemistry,  metabolism*
Macrophage Inflammatory Proteins / chemistry,  genetics,  immunology,  metabolism
Male
Mice
Mice, Inbred C57BL
Models, Molecular
Molecular Sequence Data
Mutation
Polymerization
Protein Binding
Protein Conformation
Protein Multimerization
Grant Support
ID/Acronym/Agency:
GM81539/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Chemokine CCL3; 0/Chemokine CCL4; 0/Macrophage Inflammatory Proteins; EC 3.4.24.56/Insulysin

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


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