Kapustian L. Molecular chaperone HSP60 gene expression in heart at dilated cardiomyopathy.

The object - molecular mechanisms of DCM progression. The aim of the work was the investigation of pecularities of HSP60 gene expression in the human hearts affected by DCM at the end of disease and in dynamics, using mouse model of myosin-induced autoimmune myocardial damage similar to human DCM. Applied methods - affinity chromatography, ion exchange chromatography, gel filtration chromatography, subcellular fractionation, SDS/PAAG electrophoresis, nucleic acid electrophoresis in agarose gel, Western blot analysis, polymerase chain reaction, immunofermentative analysis (ELISA), immunoprecipitation, immunohistochemical analysis. Results and novelty - the changes of Hsp60 protein and Hsp60 mRNA in heart tissue at dilated cardiomyopathy have been investigated. We have observed the increase of Hsp60 level in human hearts affected by DCM as well as in hearts of experimental mice with disease similar to human DCM. For the first time the increase of Hsp60 level in mitochondria and decrease of it in cytoplasm have been observed, which can be one of the apoptosis factors at heart failure induced by chronic stress. For the first time the presence of endogenous protein complex between Hsp60 and Bax has been revealed in the normal human heart tissue. Obtained results give us the new view on the role of molecular chaperone Hsp60 in regulation of stress-induced apoptosis, which is a key process in the progression of heart failure.