Document Detail


Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction.
MedLine Citation:
PMID:  12460879     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: We identified an interleukin-1 receptor family member, ST2, as a gene markedly induced by mechanical strain in cardiac myocytes and hypothesized that ST2 participates in the acute myocardial response to stress and injury.
METHODS AND RESULTS: ST2 mRNA was induced in cardiac myocytes by mechanical strain (4.7+/-0.9-fold) and interleukin-1beta (2.0+/-0.2-fold). Promoter analysis revealed that the proximal and not the distal promoter of ST2 is responsible for transcriptional activation in cardiac myocytes by strain and interleukin-1beta. In mice subjected to coronary artery ligation, serum ST2 was transiently increased compared with unoperated controls (20.8+/-4.4 versus 0.8+/-0.8 ng/mL, P<0.05). Soluble ST2 levels were increased in the serum of human patients (N=69) 1 day after myocardial infarction and correlated positively with creatine kinase (r=0.41, P<0.001) and negatively with ejection fraction (P=0.02).
CONCLUSIONS: These data identify ST2 release in response to myocardial infarction and suggest a role for this innate immune receptor in myocardial injury.
Authors:
Ellen O Weinberg; Masahisa Shimpo; Gilles W De Keulenaer; Catherine MacGillivray; Shin-ichi Tominaga; Scott D Solomon; Jean-Lucien Rouleau; Richard T Lee
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  106     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2002 Dec 
Date Detail:
Created Date:  2002-12-03     Completed Date:  2002-12-20     Revised Date:  2014-07-25    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2961-6     Citation Subset:  AIM; IM; S    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology
Angiotensin Receptor Antagonists
Animals
Animals, Newborn
Biological Markers / blood
Cells, Cultured
Disease Models, Animal
Gene Expression Regulation / drug effects,  physiology
Humans
Imidazoles / pharmacology
Interleukin-1 / pharmacology
Interleukin-4 / pharmacology
Lipopolysaccharides / pharmacology
Membrane Proteins / blood,  genetics,  metabolism*
Mice
Mice, Inbred C57BL
Myocardial Infarction / blood,  metabolism*
Myocardium / cytology,  metabolism*
Nuclease Protection Assays
Phorbol Esters / pharmacology
Promoter Regions, Genetic / drug effects,  physiology
Pyridines / pharmacology
RNA, Messenger / metabolism
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1
Receptors, Cell Surface
Receptors, Interleukin
Receptors, Interleukin-1 / blood,  genetics,  metabolism*
Stress, Mechanical
Stroke Volume
Grant Support
ID/Acronym/Agency:
HL052320/HL/NHLBI NIH HHS; HL63927/HL/NHLBI NIH HHS; HL69484/HL/NHLBI NIH HHS; R01 HL069484-01/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin Receptor Antagonists; 0/Biological Markers; 0/CP 191166; 0/IL1RL1 protein, human; 0/Il1rl1 protein, mouse; 0/Imidazoles; 0/Interleukin-1; 0/Lipopolysaccharides; 0/Membrane Proteins; 0/Phorbol Esters; 0/Pyridines; 0/RNA, Messenger; 0/Receptor, Angiotensin, Type 1; 0/Receptors, Cell Surface; 0/Receptors, Interleukin; 0/Receptors, Interleukin-1; 0/ST2 protein, rat; 11128-99-7/Angiotensin II; 207137-56-2/Interleukin-4
Comments/Corrections

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