title: Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction.
abstract: 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.
  
  
  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.affiliation: Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Cambridge, Mass 02139, USA.
authors.forename: Ellen O
authors.initials: EO
authors.lastname: Weinberg
authors.forename: Masahisa
authors.initials: M
authors.lastname: Shimpo
authors.forename: Gilles W
authors.initials: GW
authors.lastname: De Keulenaer
authors.forename: Catherine
authors.initials: C
authors.lastname: MacGillivray
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Tominaga
authors.forename: Scott D
authors.initials: SD
authors.lastname: Solomon
authors.forename: Jean-Lucien
authors.initials: JL
authors.lastname: Rouleau
authors.forename: Richard T
authors.initials: RT
authors.lastname: Lee
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D000831:Animals, Newborn; D015415:Biomarkers / Q000097:blood; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D000072179:Interleukin-1 Receptor-Like 1 Protein; D015847:Interleukin-4 / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008565:Membrane Proteins / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000097:blood / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D023282:Nuclease Protection Assays; D010703:Phorbol Esters / Q000494:pharmacology; D011401:Promoter Regions, Genetic / Q000187:drug effects / Q000502:physiology; D011725:Pyridines / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1; D011956:Receptors, Cell Surface; D018123:Receptors, Interleukin; D017472:Receptors, Interleukin-1 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D013314:Stress, Mechanical; D013318:Stroke Volume
chemical_list: D057911:Angiotensin Receptor Antagonists; D015415:Biomarkers; C099503:CP 191166; C079241:IL1RL1 protein, human; C486189:Il1rl1 protein, mouse; D007093:Imidazoles; D007375:Interleukin-1; D000072179:Interleukin-1 Receptor-Like 1 Protein; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D010703:Phorbol Esters; D011725:Pyridines; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D011956:Receptors, Cell Surface; D018123:Receptors, Interleukin; D017472:Receptors, Interleukin-1; C000589812:ST2 protein, rat; D000804:Angiotensin II; D015847:Interleukin-4