Document Detail


IL-4 induces protection of vascular endothelial cells against killing by complement and melittin through lipid biosynthesis.
MedLine Citation:
PMID:  20017192     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have shown previously that cytokines IL-4 and IL-13 induce protection in porcine vascular endothelial cells (EC) against killing by the membrane attack complex (MAC) of human complement. This protection is intrinsic, not due to changes in complement regulatory proteins, and requires activation of Akt and sterol receptor element binding protein-1 (SREBP-1), which regulates fatty acid and phospholipid synthesis. Here we report that, compared to EC incubated in medium, IL-4-treated EC had a profound reduction in complement-mediated ATP loss and in killing assessed by vital dye uptake, but only a slight reduction in permeability disruption measured by calcein release. While controls exposed to complement lost mitochondrial membrane potential and subsequently died, protected EC maintained mitochondrial morphology and membrane potential, and remained alive. SREBP-1 and fatty acid synthase activation were required for protection and fatty acid and phospholipid synthesis, including cardiolipin, were increased after IL-4 stimulation, without increase in cholesterol content or cell proliferation. IL-4 also induced protection of EC from killing by the channel forming protein melittin, similar to protection observed for the MAC. We conclude that IL-4 induced activation of Akt/SREBP-1/lipid biosynthesis in EC, resulting in protection against MAC and melittin, in association with mitochondrial protection.
Authors:
Sylvester M Black; Megan E Schott; Bjorn H Batdorf; Barbara A Benson; Mark S Rutherford; Brett K Levay-Young; Agustin P Dalmasso
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.    
Journal Detail:
Title:  European journal of immunology     Volume:  40     ISSN:  1521-4141     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-11     Completed Date:  2010-04-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  803-12     Citation Subset:  IM    
Affiliation:
Department of Surgery, Medical School, University of Minnesota, Minneapolis, MN 55455, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Cell Membrane Permeability
Cell Separation
Complement Membrane Attack Complex / drug effects
Complement System Proteins / drug effects*
Endothelial Cells / drug effects*,  metabolism,  ultrastructure
Flow Cytometry
Interleukin-4 / metabolism,  pharmacology*
Lipids / biosynthesis*
Melitten / adverse effects*
Membrane Potential, Mitochondrial / drug effects
Microscopy, Electron, Transmission
Mitochondria / pathology
Proto-Oncogene Proteins c-akt / drug effects,  metabolism
Signal Transduction / drug effects*
Sterol Regulatory Element Binding Protein 1 / drug effects,  metabolism
Swine
Grant Support
ID/Acronym/Agency:
R01HL062195/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Complement Membrane Attack Complex; 0/Lipids; 0/Sterol Regulatory Element Binding Protein 1; 20449-79-0/Melitten; 207137-56-2/Interleukin-4; 9007-36-7/Complement System Proteins; EC 2.7.11.1/Proto-Oncogene Proteins c-akt

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


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