|Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction.|
|PMID: 12460879 Owner: NLM Status: MEDLINE|
|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.|
|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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|Type: Journal Article; Research Support, U.S. Gov't, P.H.S.|
|Title: Circulation Volume: 106 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2002 Dec|
|Created Date: 2002-12-03 Completed Date: 2002-12-20 Revised Date: 2009-11-19|
Medline Journal Info:
|Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States|
|Languages: eng Pagination: 2961-6 Citation Subset: AIM; IM; S|
|Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Cambridge, Mass 02139, USA.|
|APA/MLA Format Download EndNote Download BibTex|
Biological Markers / blood
Disease Models, Animal
Gene Expression Regulation / drug effects, physiology
Imidazoles / pharmacology
Interleukin-1 / pharmacology
Interleukin-4 / pharmacology
Lipopolysaccharides / pharmacology
Membrane Proteins / blood, genetics, metabolism*
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
Receptor, Angiotensin, Type 1
Receptors, Angiotensin / antagonists & inhibitors
Receptors, Cell Surface
Receptors, Interleukin-1 / blood, genetics, metabolism*
|HL052320/HL/NHLBI NIH HHS; HL63927/HL/NHLBI NIH HHS; HL69484/HL/NHLBI NIH HHS; R01 HL069484-01/HL/NHLBI NIH HHS|
|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, Angiotensin; 0/Receptors, Cell Surface; 0/Receptors, Interleukin; 0/Receptors, Interleukin-1; 11128-99-7/Angiotensin II; 207137-56-2/Interleukin-4|
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