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Changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease: proteomics in human in left appendage tissue

ABSTRACT: Atrial fibrillation (AF) is the most common persistent arrhythmia that affect 1–2% of the general population. People with AF display an array of complications cardiogenic stroke and systemic embolism caused by hemodynamic instability and blood hypercoagulability in clinical practice. However, it’s still unclear whether and how ubiquitylated proteins react to AF in the left atrial appendage of patients with AF and valvular heart disease. This theory focuses on the changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease. We firstly widely analysis the proteins ubiquitination in patients with atrial fibrillation.

INSTRUMENT(S): timsTOF Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Heart

SUBMITTER: Chenkai Wu

LAB HEAD: Shenghua Zhou

PROVIDER: PXD030397 | Pride | 2021-12-24

REPOSITORIES: Pride

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Project description:Atrial fibrillation (AF) is the most common sustained arrhythmia characterized by rapid and multiple irregular excitations within the atria. AF is associated with serious morbidity and increased mortality, and its prevalence is prospected to increase as society ages. The limited therapeutic efficacy of AF treatment as well as its high socioeconomic burden makes AF a major clinical challenge. Despite our expanding knowledge of individual proteins and pathways involved in the complex pathophysiology of atrial fibrillation (AF), an unbiased overview of proteins and functionally enriched biological processes as well as their crosstalk is lacking. Here, we performed an explorative proteomics analysis to reveal the global abundance of proteins in cardiac tissue of patients, and deciphered functionally grouped gene ontologies (GO) to uncover a perspective of the disease biology driving or driven by AF. A total of 2703 proteins were identified by liquid chromatography coupled to tandem mass spectrometry. Among them, 150 proteins (accounting for 5.6% of 2703) had a significantly altered abundance (100 proteins increased and 50 decreased) in AF. A significant biological connection was found between those (protein-protein interaction enrichment p-value=1.0e-16). GO enrichment analysis showed that these 150 proteins were mainly located in extracellular/cytoplasmic vesicles, mitochondrion, and cytoskeletal compartments. Correspondingly, the 100 proteins increased in AF were significantly enriched in the GO terms related to immune system, metabolic process, iron process, ECM disassembly, mitochondrial translation and apoptotic signaling. Partially clustered proteins with dense functional link were found in immune system and metabolic process, and were respectively annotated in neutrophil degranulation, and oxoacid metabolic process coupled to the subunits of mitochondrial dehydrogenase NADH. Those processes enriched in AF had crosstalk via the proteins involved in neutrophil degranulation. Selected proteins such as LCN2 (neutrophil degranulation), CA3 (immune system), NDUFS2 (complex I) and MYH10 (actin motor protein) were validated by western blot or qPCR in an independent cohort. The 50 proteins decreased in AF were collectively enriched in vesicle-mediated transport and actin filament-based movement. We demonstrate that important biological processes underlying persistent AF as well as their crosstalk via the components of neutrophil degranulation. Our study provides a novel insight for a more efficient targeting strategy for AF treatment.

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Changes of ubiquitylated proteins in atrial fibrillation associated with heart valve disease: proteomics in human in left appendage tissue

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