Abstract 16716: Comparison of Blood Troponin I Complexes and Free Form in Acute Myocardial Infarction and End Stage Renal Disease

Introduction: Circulating blood troponin complexes and free fractions remain poorly characterised in different conditions where troponin is detectable in blood Hypothesis: The aim of the study was to compare the differences in troponin-I(TnI) complexes/free-forms in end stage renal disease (ESRD) compared to acute myocardial infarction(AMI) Methods: Blood was collected from patients with AMI(n=7) or ESRD(n=4) at two time points (a)As early as possible after AMI or at initial contact with ESRD patients and (b)24-48 hours later. Western blotting was carried out with HyTest cTnI-560cc antibody on plasma extracted from whole blood. Densitometry analysis was performed and evaluated using the independent samples T-test and paired T-test as appropriate Results: Prominent bands were noted at ~45,~37 and ~25 kDa respectively representing low molecular weight(LMW) TnI-TnT-TnC complex, binary TnI-TnC complex and free-TnI. At time-point (a), there was no difference in these bands between STEMI and CKD patients. Interestingly, at time-point (b), AMI patients had significantly lower intensity of the 45kDa and 37kDa bands compared to CKD patients(for 45 kDa band mean difference was 54.3±19.4 AU, p=0.02; for 37 kDa band mean difference was 27.7±10.5 AU, p=0.03) as well as compared to the initial STEMI samples taken at time-point (a)(for 45 kDa band mean difference was 41.4±8.1 AU, p=0.002; for 37 kDa band mean difference was 16.7±6.3 AU, p=0.002) ,however there was no difference in the 25kDa band Conclusions: AMI patients had progressively lesser quantities of circulating LMW-ITC and binary IC complexes following AMI compared to ESRD patients, but similar quantities of circulating free TnI. This indicates a constant release of LMW-ITC and binary-IC complexes from the myocardium or reduced glomerular filtration of these complexes in ESRD while in the AMI patients, the LMW-ITC and binary I-C complexes appear to be progressively eliminated from plasma after the initial release </jats:p

Cardiac expression of microRNA-7 is associated with adverse cardiac remodeling

AbstractAlthough microRNA-7 (miRNA-7) is known to regulate proliferation of cancer cells by targeting Epidermal growth factor receptor (EGFR/ERBB) family, less is known about its role in cardiac physiology. Transgenic (Tg) mouse with cardiomyocyte-specific overexpression of miRNA-7 was generated to determine its role in cardiac physiology and pathology. Echocardiography on the miRNA-7 Tg mice showed cardiac dilation instead of age-associated physiological cardiac hypertrophy observed in non-Tg control mice. Subjecting miRNA-7 Tg mice to transverse aortic constriction (TAC) resulted in cardiac dilation associated with increased fibrosis bypassing the adaptive cardiac hypertrophic response to TAC. miRNA-7 expression in cardiomyocytes resulted in significant loss of ERBB2 expression with no changes in ERBB1 (EGFR). Cardiac proteomics in the miRNA-7 Tg mice showed significant reduction in mitochondrial membrane structural proteins compared to NTg reflecting role of miRNA-7 beyond the regulation of EGFR/ERRB in mediating cardiac dilation. Consistently, electron microscopy showed that miRNA-7 Tg hearts had disorganized rounded mitochondria that was associated with mitochondrial dysfunction. These findings show that expression of miRNA-7 in the cardiomyocytes results in cardiac dilation instead of adaptive hypertrophic response during aging or to TAC providing insights on yet to be understood role of miRNA-7 in cardiac function.</jats:p

β-Arrestins: Multitask Scaffolds Orchestrating the Where and When in Cell Signalling

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