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 assessed changes in mitochondrial NADH as autofluorescence in myocytes. Consistent with previous results,19 addition of H2O2 significantly increased NADH signal that could be attenuated with nisoldipine (Figure 5A and 5B). Collapse of the signal with addition of NaCN indicated that the signal was mitochondrial in origin. Application of 1 and 10 μmol/L of AID‐TAT peptide attenuated the increase in NADH associated with application of H2O2 (Figure 5C and 5D). This suggested that AID‐TAT peptide was altering NADH as a result of effects on MMP or oxygen consumption.
Affiliation: School of Anatomy, Physiology and Human Biology, The University of Western Australia, Crawley, WA, Australia (H.M.V., L.C.H.).