Left ventricular unloading alters receptor tyrosine kinase expression in the failing human heart.

摘要: Abstract Background: Experimental and clinical data suggest that the loss of membrane receptor tyrosine kinase (RTK) activity in cardiac myocytes results increased frequency apoptotic cell death progression heart failure. The goal our study was to examine expression characteristics RTKs ventricular myocardium obtained from patients before after mechanical unloading. Methods: We extracted RNA paired formalin-fixed, paraffin-embedded left tissue blocks at time assist device (LVAD) implantation explantation a cohort 36 (median age 51 years). duration LVAD support ranged 1 314 days 95 days), 17 had ischemic 19 non-ischemic cardiomyopathy implantation. Using real-time reverse transcription–polymerase chain reaction (RT-PCR) we quantitated transcripts for atrial natriuretic factor (ANF) tumor necrosis factor-alpha (TNF-α), markers failure, Her2/neu, Her4 gp130, regulators survival. Results: In undergoing unloading, ANF TNF-α mRNA levels were independently suppressed. along with upregulated, mostly cases cardiomyopathy, whereas gp130 decreased. Post-LVAD transcript Her2 correlated tightly non-pathologic entry values gp130. Duration treatment also determining factors change these genes. Conclusion: Real-time quantitative (Q)-RT-PCR can be used quantitate gene archival myocardial blocks. Mechanical unloading leads re-adjustment RTK levels, but not their reverting control failure patients.