Document Detail


Chronic treatment of mice with leukemia inhibitory factor does not cause adverse cardiac remodeling but improves heart function.
MedLine Citation:
PMID:  23291613     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent evidence suggests that the IL-6 family cytokine, leukemia inhibitory factor (LIF) is produced by cardiac cells under stress conditions including myocardial infarction and heart failure. Additionally, short-term delivery of LIF has been shown to have preconditioning effects on the heart and to limit infarct size. However, cell culture studies have suggested that LIF may exert harmful effects on cardiac myocytes, including pathological hypertrophy and contractile dysfunction. Long-term effects of LIF on the heart in vivo have not been reported and were the focus of this study. Adult male mice were injected daily with LIF (2 μg/30 g) or saline for 10 days. LIF treatment caused an approximate 11% loss in body weight. Cardiac function as assessed by echocardiography was improved in LIF-treated mice. Ejection fraction and fractional shortening were increased by 21% and 32%, respectively. No cardiac hypertrophy was seen on histology in LIF-treated mice,, there was no change in the heart-to-tibia length ratio, and no cardiac fibrosis was observed. STAT3 was markedly activated by LIF in the left ventricle. Different effects of LIF were seen in protein levels of genes associated with STAT3 in the left ventricle: levels of SOD2 and Bcl-xL were unchanged, but levels of total STAT3 and MCP-1 were increased. There was a trend towards increased expression of miR-17, miR-21, and miR-199 in the left ventricle of LIF-treated mice, but these changes were not statistically significant. In conclusion, effects of chronic LIF treatment on the heart, although modest, were positive for systolic function: adverse cardiac remodeling was not observed. Our findings thus lend further support to recent proposals that LIF may have therapeutic utility in preventing injury to or repairing the myocardium.
Authors:
Carlos Zgheib; Fouad Anthony Zouein; Mazen Kurdi; George Warren Booz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European cytokine network     Volume:  23     ISSN:  1952-4005     ISO Abbreviation:  Eur. Cytokine Netw.     Publication Date:    2012 Oct-Dec
Date Detail:
Created Date:  2013-02-08     Completed Date:  2013-07-30     Revised Date:  2013-11-06    
Medline Journal Info:
Nlm Unique ID:  9100879     Medline TA:  Eur Cytokine Netw     Country:  France    
Other Details:
Languages:  eng     Pagination:  191-7     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, School of Medicine, and the Center for Excellence in Cardiovascular-Renal Research, The University of Mississippi Medical Center, Jackson, Mississippi, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomegaly / enzymology,  genetics,  pathology,  physiopathology
Chemokine CCL2 / metabolism
Fibrosis
Gene Expression Regulation / drug effects
Heart / drug effects*,  physiopathology*
Heart Function Tests / drug effects*
Leukemia Inhibitory Factor / pharmacology*
Male
Mice
Mice, Inbred C57BL
MicroRNAs / genetics,  metabolism
STAT3 Transcription Factor / metabolism
Staining and Labeling
Stroke Volume / drug effects
Superoxide Dismutase / metabolism
Ventricular Remodeling / drug effects*
bcl-X Protein / metabolism
Grant Support
ID/Acronym/Agency:
R01 HL088101/HL/NHLBI NIH HHS; R01HL088101-06/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/CCL2 protein, human; 0/Chemokine CCL2; 0/Leukemia Inhibitory Factor; 0/Lif protein, mouse; 0/MicroRNAs; 0/STAT3 Transcription Factor; 0/bcl-X Protein; EC 1.15.1.1/Superoxide Dismutase; EC 1.15.1.1/superoxide dismutase 2
Comments/Corrections

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