Elevated Plasma Level Of Cardiac-Specific Map Kinase Tnni3k In Acute Myocardial Infarction And Its Significance

Aims: TNNI3K is a cardiac-specifically expressed MAP kinase in both embryonic and adult and localizes in cytoplasm and in nucleus. Our recent study indicated TNNI3K can specifically interact with cardiac troponin I and plays important roles including cardiac myogenesis promotion, cardiac performance enhancement, and reduction of myocardial ischemic injury by suppressing p38/JNK-mediated apoptosis. The aim of this study is to evaluate whether plasma TNNI3K levels can predict the occurrence of acute cardiac infarction (AMI). Methods and results: Polyclonal anti-human TNNI3K antibody was raised in rabbit by injecting recombinant TNNI3K and purified as IgG by using protein A-conjugated sepharose column. The antibody did not react with human plasma proteins in healthy volunteers by Western blotting and reacted with TNNI3K over-expressed in P19CL6 pluripotent cells-derived cardiac myocytes by immunostaining. Standard curve gained by enzyme-linked immunosorbent assay (ELISA) was linear through the range from 0.011 to 11.00 ng/ml of TNNI3K protein. Plasma TNNI3K concentrations of healthy volunteers, acute renal failure, chronic heart failure and acute myocardial infarct patients measured by ELISA were 221.38±12.8 (n=21), 218.26±6.8 (n=6), 320.7±8.9 (n=18) and 2025.0±200.7 (n=10) ng/ml, respectively. Circulating TNNI3K level in acute myocardial infraction was significantly higher than that in any other group (p Conclusions: Measurement of circulating TNNI3K level may be a novel useful diagnostic tool for acute myocardial infarction. Related patents were applied (WO2006057278; US20090022692; EP1832299).