Decreased myocardial injury and improved contractility after administration of a peptide derived against the alpha-interacting domain of the L-type calcium channel.
Bottom Line: Activation of the channel also alters mitochondrial function.In search of the mechanism for the effect, we found that intracellular calcium ([Ca(2+)]i, Fura-2), superoxide production (dihydroethidium fluorescence), mitochondrial membrane potential (Ψm, JC-1 fluorescence), reduced nicotinamide adenine dinucleotide production, and flavoprotein oxidation (autofluorescence) are decreased after application of AID-TAT peptide.Application of AID-TAT peptide significantly decreased infarct size and supported contractility up to 12 weeks postcoronary artery occlusion as a result of a decrease in metabolic demand during reperfusion.
Affiliation: School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, WA, Australia (H.M.V., L.C.H.).Show MeSH
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Mentions: We examined the effect of a single application of 1 μmol/L of AID‐TAT peptide injected into the coronaries through the aorta within 5 minutes after commencement of reperfusion in hearts exposed to 30 minutes of no‐flow ischemia on a Langendorff apparatus. In hearts exposed to active peptide, infarct size was significantly decreased, compared to hearts exposed to 1 μmol/L of scrambled peptide (AID(S)‐TAT) (Figure 1A and 1B). Release of CK (Figure 1C) and LDH (Figure 1D) was significantly less in hearts exposed to active peptide. However, the ratio of GSH/GSSG was not altered after administration of 1 μmol/L of AID‐TAT. When the concentration of the active peptide was increased to 10 μmol/L, GSH increased, suggesting an attenuation of OS (Figure 1E).
Affiliation: School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, WA, Australia (H.M.V., L.C.H.).