PXD050441-1

PXD050441 is an original dataset announced via ProteomeXchange.

Title	Ischemic preconditioning predominantly affects phosphosites involved in myocardial contraction and promotes myocardial stunning while reducing infarction size in rats.
Description	Background: Ischemic preconditioning (IPC), i.e., brief periods of ischemia, protect the heart from subsequent prolonged ischemic injury, and reduces infarction size. Myocardial stunning refers to transient loss of contractility in the heart after myocardial ischemia that recovers without causing permanent damage. The relationship between IPC and myocardial stunning remains incompletely understood. Purpose: The primary aim of this study was to examine the effects of IPC on the relationship between ischemia duration, stunning, and infarct size in an ischemia-reperfusion injury model. The secondary aim of the study was to examine to which extent the phosphoproteomic changes induced by IPC relate to myocardial contractile function. Methods: Rats were subjected to different durations of left anterior descending artery (LAD) occlusion, with or without preceding IPC. Echocardiograms were acquired at 4 and 48 hours to assess cardiac contraction in the affected myocardial segment. Reversible akinesia was defined as the presence of myocardial akinesia at 4 hours that resolved by 48 hours; and was considered to represent myocardial stunning. Infarction size was evaluated using triphenyl tetrazolium chloride staining. Phosphoproteomic analysis was performed in heart tissue from preconditioned and non-preconditioned animals using nano-liquid chromatography-mass spectrometry. Results: Reversible akinesia was observed in a majority of the rats that were subjected to IPC and subsequently exposed to ischemia of 13.5 or 15 minutes of ischemia (83.3% [n/N] and 66.6% [n/N] respectively). Among rats without IPC, who were exposed to either 10, 11, 12 or 13.5 minutes of ischemia, reversible akinesia was observed in 0% (n/N), 17% (2/12), 0% (n/N) and 0% (n/N) of rats (p<0.001). Phosphoproteomic analysis revealed significant differential regulation of 809 phosphopeptides between IPC and non-IPC groups, with significant associations with the sarcomere, Z-disc, and actin binding. Conclusion: Our study shows that IPC preferentially induces changes in phosphosites of proteins involved in myocardial contraction, and both increases the incidence of reversible post-ischemic myocardial stunning after ischemia-reperfusion injury and reduces infarction size.
HostingRepository	PRIDE
AnnounceDate	2024-05-15
AnnouncementXML	Submission_2024-05-15_04:07:57.551.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Evelin Berger
SpeciesList	scientific name: Rattus norvegicus (Rat); NCBI TaxID: 10116;
ModificationList	methylthiolated residue; phosphorylated residue; monohydroxylated residue
Instrument	Orbitrap Fusion Lumos

Revision	Datetime	Status	ChangeLog Entry
0	2024-03-07 06:01:58	ID requested
⏵ 1	2024-05-15 04:07:58	announced

Elmahdy A, Shekka Espinosa A, Kakaei Y, Pylova T, Jha A, Zulfaj E, Krasnikova M, Al-Awar A, Sheybani Z, Sevastianova V, Berger E, Nejat A, Molander L, Andersson EA, Omerovic E, Hussain S, Redfors B, Ischemic preconditioning affects phosphosites and accentuates myocardial stunning while reducing infarction size in rats. Front Cardiovasc Med, 11():1376367(2024) [pubmed]

10.3389/fcvm.2024.1376367;

submitter keyword: Myocardial infarction, Phosphoproteomics, Ischemic preconditioning, Echocardiography, Speckle tracking analysis, Myocardial stunning

Carina Sihlbom Wallem
contact affiliation	Proteomics Core Facility, Sahlgrenska Academy, University of Gothenburg, Sweden
contact email	carina.sihlbom@gu.se
lab head
Evelin Berger
contact affiliation	Proteomics Core Facility, University of Gothenburg
contact email	evelin.berger@gu.se
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD050441
     1. Label: PRIDE project
     2. Name: Ischemic preconditioning predominantly affects phosphosites involved in myocardial contraction and promotes myocardial stunning while reducing infarction size in rats.