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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction.

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.[1]

References

  1. Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction. Weinberg, E.O., Shimpo, M., De Keulenaer, G.W., MacGillivray, C., Tominaga, S., Solomon, S.D., Rouleau, J.L., Lee, R.T. Circulation (2002) [Pubmed]
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