Complement Factor MASP-2 is activated after acute myocardial ischemia in human (116.28)

• Published in: The Journal of immunology (1950) 2011-04, Vol.186 (1_Supplement), p.116-116.28
• Main Authors: Zhang, Ming, Hou, Yunfang, Cavusoglu, Erdal, Lee, Daniel, Steffensen, Rudi, Yang, Liming, Jensenius, Jens, Marmur, Jonathan, Schwaeble, Wilhelm, Ko, Wilson, Shevde, Ketan
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.186.Supp.116.28

Acute blockage of coronary artery results in myocardial injury manifested in clinical situations such as myocardial infarction (MI). Following ischemia, inflammation is provoked and may be related to the clinical outcomes. We studied the acute inflammatory response immediately following myocardial ischemia in human. Our results showed that in acute MI patients circulation levels of complement factor MASP-2 were significantly reduced comparing with those of healthy individuals or of coronary artery disease (CAD) patients without acute MI. This reduction was not due to genetic polymorphism of MASP-2 in acute MI patients. We hypothesized that MASP-2 was activated after acute myocardial ischemia, and tested this in cardiac patients undergoing surgically induced transient global heart ischemia. Our results showed that MASP-2 was significantly reduced in coronary circulation after global heart ischemia and was independently correlated with the post-operative increase of the myocardial injury marker, cardiac Troponin I. These data suggested that MASP-2 is activated in human acute heart ischemia and associated with myocardial injury.