Significances of modifying TNNI3 function by overexpression of MAP kinase TNNI3K

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TNNI3K is a MAP kinase specifically and continuouslyexpressed in cardiac muscle and interacted with cardiac troponin I (TNNI3, or: cTnI). The aim of this study is to investigate role of TNNI3K interacting with cTnI on modification the physiological function of cardiomyocytes, suppressing some pathological injuries and to explain the new molecular mechanism for TNNI3K-mutant in the ischemic coronary heart diseases, and hope to develop some new therapeutic strategies. In the in vitro experiments, 1) Effects of PKC inhibitor (GF109203X) or PKA activator (Br-8-cAMP) on the beating frequency were investigated in P19CL6-derived culture beating cardiomyocytes. Results showed that TNNI3K-overexpression increased the contractility and beating frequency together with restrained phosphorylation of cTnI through activation of the PKA pathway but not by blocking of the PKC pathway. 2) Availability of plasma TNNI3K level was investigated using with anti-TNNI3K poly-antibodies in patients diagnosed as AMI (n=40), chronic heart failure (CHF, n=18) and acute renal failure (ARF, n=6); and in healthy volunteers (n=12). Data shown that circulating TNNI3K levels were significantly higher in AMI (p