Document Detail


Mesenchymal stem cells attenuate myocardial functional depression and reduce systemic and myocardial inflammation during endotoxemia.
MedLine Citation:
PMID:  20434747     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Endotoxemia is associated with depressed cardiac function during sepsis. Mesenchymal stem cells (MSCs) possess an ability to modulate the inflammatory response during sepsis, but it is unknown whether MSCs possess the ability to reduce endotoxemia-induced myocardial injury and dysfunction. METHODS: Endotoxemia was induced in rats via injection of lipopolysaccharide (LPS). Animals were divided into the following groups: (1) saline + saline; (2) LPS + saline; (3) LPS + MSCs; and (4) LPS + LLC-PK1 renal epithelial cells (differentiated control). At 6 hours, animals were anesthetized, serum was collected, and hearts were extracted and perfused via the isolated heart system. Hearts and serum were analyzed for tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-10. RESULTS: The administration of LPS depressed myocardial function. Treatment with MSCs ameliorated this depression. Serum TNF-alpha, IL-1beta, and IL-6 were elevated in LPS-treated groups. Treatment with MSCs was associated with reduced levels of these cytokines. A trend toward reduced myocardial TNF-alpha and significant reductions in myocardial IL-1beta and IL-6 were observed in the MSC-treated group. IL-10 levels were increased after the LPS administration in both serum and myocardium. Serum levels were increased further after treatment with MSCs. CONCLUSION: Treatment with MSCs during endotoxemia reduces systemic and myocardial inflammation and is associated with a reduction in LPS-induced myocardial functional depression.
Authors:
Brent R Weil; Mariuxi C Manukyan; Jeremy L Herrmann; Yue Wang; Aaron M Abarbanell; Jeffrey A Poynter; Daniel R Meldrum
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Surgery     Volume:  148     ISSN:  1532-7361     ISO Abbreviation:  Surgery     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-16     Completed Date:  2010-08-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0417347     Medline TA:  Surgery     Country:  United States    
Other Details:
Languages:  eng     Pagination:  444-52     Citation Subset:  AIM; IM    
Copyright Information:
Copyright 2010 Mosby, Inc. All rights reserved.
Affiliation:
Department of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal
Endotoxemia / immunology,  pathology,  physiopathology,  therapy*
Heart / drug effects,  physiopathology*
Inflammation / immunology,  pathology,  therapy
Interleukin-10 / biosynthesis
Interleukin-1beta / metabolism
Interleukin-6 / metabolism
Lipopolysaccharides / toxicity
Macrophages / physiology
Male
Mesenchymal Stem Cell Transplantation*
Mesenchymal Stem Cells / physiology
Myocarditis / immunology,  pathology,  therapy
Rats
Rats, Sprague-Dawley
Tumor Necrosis Factor-alpha / metabolism
Grant Support
ID/Acronym/Agency:
F32HL092718/HL/NHLBI NIH HHS; F32HL092719/HL/NHLBI NIH HHS; F32HL093987/HL/NHLBI NIH HHS; R01GM070628/GM/NIGMS NIH HHS; R01HL085595/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Interleukin-1beta; 0/Interleukin-6; 0/Lipopolysaccharides; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10

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


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