Circulation · 2002
Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction.
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Weinberg Ellen O, Shimpo Masahisa, De Keulenaer Gilles W, MacGillivray Catherine, Tominaga Shin-ichi, Solomon Scott D, Rouleau Jean-Lucien, Lee Richard T
Аннотация
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.
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.
Предметные рубрики MeSH
Angiotensin IIAngiotensin Receptor AntagonistsAnimalsAnimals, NewbornBiomarkersCells, CulturedDisease Models, AnimalGene Expression RegulationHumansImidazolesInterleukin-1Interleukin-1 Receptor-Like 1 ProteinInterleukin-4LipopolysaccharidesMembrane ProteinsMiceMice, Inbred C57BLMyocardial InfarctionMyocardiumNuclease Protection AssaysPhorbol EstersPromoter Regions, GeneticPyridinesRNA, MessengerRatsRats, Sprague-DawleyReceptor, Angiotensin, Type 1Receptors, Cell SurfaceReceptors, InterleukinReceptors, Interleukin-1Stress, MechanicalStroke Volume