Key result
Proteomic analysis of rats with experimental autoimmune myocarditis-induced chronic heart failure identified increased expression of proteins such as GRP78 and HSP90 beta that strongly correlated with cardiac dysfunction.
Proteomic analysis of an autoimmune myocarditis-induced heart failure rat model identified GRP78 and HSP90beta as proteins highly correlated with cardiac dysfunction, suggesting they may be novel therapeutic targets.
Hypothesis-generating in rat myocarditis model; leaves open whether GRP78 or HSP90beta are viable human therapeutic targets.
Experimental autoimmune myocarditis (EAM)-induced heart failure in rats is used to study the pathogenesis of heart failure. Based on a proteomic analysis of soluble (S) and membranous (M) fractions extracted from ventricles of rats with a stable chronic form of EAM-induced heart failure, we assessed changes in protein levels and their correlation to heart functions to gain insights into the pathogenesis and to explore new targets for the treatment of heart failure. Proteins were separated by two-dimensional gel electrophoresis and silver stained spots were analyzed. In the S-fraction, 274+/-3 spots were detected in the normal (N)-group and 273+/-6 in the heart failure (HF)-group. In the HF-group, 26 of the spots were increased and 15 were decreased in intensity. In the M-fraction, 277+/-3 spots were detected in the N-group and 277+/-2 in the HF-group, with 20 spots increased and 10 decreased in intensity. We analyzed relationships between the expression of these proteins and 11 parameters of heart function, and found all the significantly changed spots to correlate with at least one of the parameters. We analyzed 49 spots that correlated with over 9 parameters of heart function using mass spectrometry, and identified 15 as proteins with increased expression including glucose regulated protein (GRP)78, an endoplasmic-stress related protein, and heat shock protein (HSP)90beta, a molecular chaperone, and 4 spots as proteins with decreased expression. It is suggested that in the heart failure model, GRP78 and HSP90beta play a role in the protection or deterioration of the heart and may be new targets for treatment.
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Sanzen et al. (2010) studied Experimental autoimmune myocarditis-induced chronic heart failure (n=20). Experimental autoimmune myocarditis induction vs. Normal age-matched rats was evaluated on Protein expression changes correlated with heart function. Proteomic analysis of rats with experimental autoimmune myocarditis-induced chronic heart failure identified increased expression of proteins such as GRP78 and HSP90 beta that strongly correlated with cardiac dysfunction.
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