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 AID‐TAT peptide on contractility ex vivo in hearts exposed to ischemia then reperfusion. In hearts exposed to scrambled peptide, developed pressure decreased during reperfusion and did not improve during the 30 minutes after ischemia (Figure 2A and 2B). Application of 1 μmol/L of AID‐TAT had no effect on postischemia recovery; however, 10 μmol/L of AID‐TAT significantly improved developed pressure 20 to 30 minutes after ischemia (Figure 2D and 2E). Application of 10 μmol/L of AID‐TAT peptide did not alter developed pressure over 60 minutes in the absence of I/R (Figure 2E).
Affiliation: School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, WA, Australia (H.M.V., L.C.H.).