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Phosphoproteomic and proteomic profiling in post-infarction chronic heart failure

ABSTRACT: We conducted a global quantitative phosphoproteomic and proteomic analysis of left ventricular (LV) tissues from post-infarction chronic heart failure rats. Phosphoproteomic and proteomic analysis can provide insights regarding molecular mechanisms underlying post-infarction chronic heart failure and explore new therapeutic approaches.

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Xiao Lu

PROVIDER: PXD042843 | iProX | Fri Jun 09 00:00:00 BST 2023

REPOSITORIES: iProX

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Phosphoproteomic and proteomic profiling in post-infarction chronic heart failure.

Wang Jiayue J Zhu Xiuhua X Wang Shenrui S Zhang Yingjie Y Hua Wenjie W Liu Zhenyu Z Zheng Yu Y Lu Xiao X

Frontiers in pharmacology 20230619

<b>Background:</b> Post-infarction chronic heart failure is the most common type of heart failure. Patients with chronic heart failure show elevated morbidity and mortality with limited evidence-based therapies. Phosphoproteomic and proteomic analysis can provide insights regarding molecular mechanisms underlying post-infarction chronic heart failure and explore new therapeutic approaches. <b>Methods and results:</b> Global quantitative phosphoproteomic and proteomic analysis of left ventricular ...[more]

PMID: 37405054

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Project description:Full Title: Transition from Compensated Hypertrophy to Systolic Heart Failure in the Spontaneously Hypertensive Rat: Structure, Function, and Transcript Analysis Gene expression changes and left ventricular remodeling associated with the transition to systolic heart failure (HF) were determined in the spontaneously hypertensive rat (SHR). By combining transcriptomics of left ventricles from six SHR with HF with changes in function and structure we aimed to better understand the molecular events underlying the onset of systolic HF compared to six age-matched, SHR with compensated hypertrophy. Left ventricle (LV) ejection fraction was depressed (82Â±4 to 52Â±3 %) in compensated vs. failing animals.Â Systolic blood pressure decreased and LV end-diastolic and systolic volume increased with HF.Â Failing SHR hearts also demonstrated increases in left and right ventricular mass relative to non-failing SHRs.Â Â LV papillary muscle force development and shortening velocity decreased, Î²-adrenergic responsiveness was depressed, myocardial stiffness and myocardial fibrosis increased with HF relative to non-failing animals. Initial micro-array analysis revealed that 1,431 transcripts were differentially expressed with HF compared to non-failing SHR (p<0.05). Of the identified transcripts, lipopolysaccharide binding protein, the most highly expressed transcript with HF, was negatively correlated to myocardial force while elevated expression of the collagen cross-linking enzyme lysyl oxidase correlated positively with muscle stiffness. Besides these individual transcripts, gene set enrichment analysis (GSEA) identified multiple enriched pathways with HF, most prominent of the altered signaling pathways involved TGF-Î² and insulin signaling. GESA analysis additionally identified altered gene sets involving inflammation, oxidative stress, cell degradation and cell death, among others (all p<0.01). In contrast to diastolic HF where few transcripts are reported to be altered, our data indicate multiple genes and pathways involved in a variety of biological processes characterize the onset of systolic HF, consistent with many functional and structural changes present in the failing hypertensive heart. Comprehensive gene expression profiling of heart failure Rat model vs control.

Dataset Information

Phosphoproteomic and proteomic profiling in post-infarction chronic heart failure

Publications

Phosphoproteomic and proteomic profiling in post-infarction chronic heart failure.

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