Proteomics

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Mouse Heart SS31 Targeted Proteomics


ABSTRACT: The S-glutathionylation and phosphorylation proteomes of mouse hearts were analyzed using shotgun proteomics methods in order to assess the effects of aging and the ability of mitochondrion-targeted drug SS-31 to reverse age-related changes. There was a nearly universal increase in S-gluthationylation of cysteine residues on proteins taken from Old (24 months old at the start of the study) mouse hearts compared to Young (5-6 months old). This shift in proteome oxidation state was almost completely reversed by 8-weeks of SS-31 treatment. Many of the significant changes that occurred were in mitochondrial pathways. Changes in phosphorylation did not show a clear pattern, as there was a mix of enhancement and suppression of phosphorylation with age among different proteins. SS-31 showed some effect at restoring the phosphorylation state of proteins that had increased phosphorylation with age but it had no effect on those that had decreased phosphorylation with age. A subset of phosphorylation sites was also analyzed by parallel reaction monitoring, which revealed that Myot S231 had a change in the proportion of phosphorylated and unphosphorylated proteins and that cMyBP-C S307 had a proportional increase in phosphorylated and unphosphorylated protein with age, but that SS-31 treatment did not affect these changes.

ORGANISM(S): Mus Musculus

SUBMITTER: Gennifer Merrihew  

PROVIDER: PXD024247 | panorama | Wed Mar 16 00:00:00 GMT 2022

REPOSITORIES: PanoramaPublic

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Publications


It has been demonstrated that elamipretide (SS-31) rescues age-related functional deficits in the heart but the full set of mechanisms behind this have yet to be determined. We investigated the hypothesis that elamipretide influences post-translational modifications to heart proteins. The S-glutathionylation and phosphorylation proteomes of mouse hearts were analyzed using shotgun proteomics to assess the effects of aging on these post-translational modifications and the ability of the mitochond  ...[more]

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