Document Detail


Dynamics of activation of lecithin:cholesterol acyltransferase by apolipoprotein A-I.
MedLine Citation:
PMID:  19860440     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The product of transesterification of phospholipid acyl chains and unesterified cholesterol (UC) by the enzyme lecithin:cholesterol acyltransferase (LCAT) is cholesteryl ester (CE). Activation of LCAT by apolipoprotein (apo) A-I on nascent (discoidal) high-density lipoproteins (HDL) is essential for formation of mature (spheroidal) HDL during the antiatherogenic process of reverse cholesterol transport. Here we report all-atom and coarse-grained (CG) molecular dynamics (MD) simulations of HDL particles that have major implications for mechanisms of LCAT activation. Both the all-atom and CG simulations provide support for a model in which the helix 5/5 domains of apoA-I create an amphipathic "presentation tunnel" that exposes methyl ends of acyl chains at the bilayer center to solvent. Further, CG simulations show that UC also becomes inserted with high efficiency into the amphipathic presentation tunnel with its hydroxyl moiety (UC-OH) exposed to solvent; these results are consistent with trajectory analyses of the all-atom simulations showing that UC is being concentrated in the vicinity of the presentation tunnel. Finally, consistent with known product inhibition of CE-rich HDL by CE, CG simulations of CE-rich spheroidal HDL indicate partial blockage of the amphipathic presentation tunnel by CE. These results lead us to propose the following working hypothesis. After attachment of LCAT to discoidal HDL, the helix 5/5 domains in apoA-I form amphipathic presentation tunnels for migration of hydrophobic acyl chains and amphipathic UC from the bilayer to the phospholipase A2-like and esterification active sites of LCAT, respectively. This hypothesis is currently being tested by site-directed mutagenesis.
Authors:
Martin K Jones; Andrea Catte; Ling Li; Jere P Segrest
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Biochemistry     Volume:  48     ISSN:  1520-4995     ISO Abbreviation:  Biochemistry     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-25     Completed Date:  2009-12-17     Revised Date:  2011-03-03    
Medline Journal Info:
Nlm Unique ID:  0370623     Medline TA:  Biochemistry     Country:  United States    
Other Details:
Languages:  eng     Pagination:  11196-210     Citation Subset:  IM    
Affiliation:
Department of Medicine and Atherosclerosis Research Unit, University ofAlabama, Birmingham, Alabama 35294, USA.
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MeSH Terms
Descriptor/Qualifier:
Apolipoprotein A-I / chemistry,  metabolism*
Catalytic Domain
Cholesterol / chemistry,  metabolism
Cholesterol Esters / chemistry,  metabolism
Computer Simulation
Enzyme Activation
Esterification
Hydrophobic and Hydrophilic Interactions
Lipid Bilayers / chemistry,  metabolism
Lipoproteins, HDL / chemistry,  metabolism
Models, Molecular
Phosphatidylcholine-Sterol O-Acyltransferase / chemistry,  metabolism*
Protein Binding
Protein Structure, Secondary
Grant Support
ID/Acronym/Agency:
P01 HL-34343/HL/NHLBI NIH HHS; P01 HL034343-22/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Apolipoprotein A-I; 0/Cholesterol Esters; 0/Lipid Bilayers; 0/Lipoproteins, HDL; 57-88-5/Cholesterol; EC 2.3.1.43/Phosphatidylcholine-Sterol O-Acyltransferase

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


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