In LV tissues, protein expressions of inflammatory (tumor-necrosis factor-α/nuclear-factor-κB/interleukin-1ß/matrix-metalloprotianse-9), oxidative stress (NOX-1/NOX-2/oxidized protein), apoptotic (mitochondrial-Bax/cleaved-caspase-3/cleaved-PARP), fibrotic (transforming-growth factor-ß/Smad3), DNA/mitochondrial-damage (γ-H2AX/cytosolic-cytochrome-C) and heart failure (brain natriuretic peptide (BNP) levels displayed an opposite pattern to LVEF among the three groups (all p < 0.0001).
<b>Conclusion:</b> Tand-scFv<sub>Sca-1+GPIIb/IIIa</sub> is a promising candidate to enhance therapeutic cell delivery in order to promote myocardial regeneration and thereby preventing heart failure.
The mRNA and protein expression levels of caspase‑3 and Bcl‑2‑associated X protein were decreased in the CHF‑VNS group, the expression of Birc2 and B‑cell lymphoma 2 were increased.
Ingenuity Pathway Analysis indicated that cross-talk among several key nodal molecules (e.g. cyclin-dependent kinase inhibitor 1A, caspase-3, nuclear factor kappa-light-chain enhancer of activated B cells etc.) may play a regulatory role in the transition of CH to HF.
Caspase 3 activation in heart failure sequentially cleaved SRF and generated a dominant-negative transcription factor, which may explain the depression of cardiac-specific genes.