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Circulating Proteome Profiling Identifies the Hub Proteins and Biological Processes in Ischemic and Non-ischemic Dilated Cardiomyopathy

ABSTRACT: The following three groups of 15 subjects were selected for TMT quantitative proteome analysis and identification of differentially expressed proteins. Group A: 5 patients with ischemic cardiomyopathy caused by myocardial infarction; group B: 5 patients with non ischemic dilated cardiomyopathy; group C: 5 healthy controls. ITRAQ method was used for quantitative proteomic analysis of TMT and identification of differentially expressed proteins. The main detection contents include: total protein extraction, protein quality inspection, TMT labeling, fraction separation, TMT quantitative proteomic mass spectrometry detection and analysis, protein function analysis and differential protein quantitative analysis and identification.

ORGANISM(S): Homo Sapiens

SUBMITTER: Guangyong Huang

PROVIDER: PXD028101 | iProX | Tue Aug 24 00:00:00 BST 2021

REPOSITORIES: iProX

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Project description:Aims Ischemic cardiomyopathy with comorbid sleep apnea syndrome (SAS) is associated with worse long-term outcomes. Intermittent hypoxia (IH), a key feature of SAS, exacerbates sympathetic activity, hastening cardiac dysfunction and remodeling in ischemic cardiomyopathy rat models. This study explores whether targeted cardiac sympathetic denervation (CSD) can limit IH-induced progression of ischemic cardiomyopathy. Methods and results Male Wistar rats underwent myocardial infarction (MI) via permanent left coronary artery ligation, and CSD was simultaneously achieved through ablation of the left middle cervical and stellate ganglions. Rats were exposed to IH (21–5% fraction of inspired O2, 60 s cycle, 8 h/day) or normoxia (N) for 14 weeks starting 3 days post-surgery. Throughout the intervention period, cardiac sympathetic activity was assessed using spectral analysis of heart rate variability (HRV) from vigil ECG collected with a specialized jacket. Cardiac function and remodeling were monitored via echocardiography. Additionally, isolated cardiomyocytes from rats exposed to IH or N for 6 weeks were assessed for calcium transient, sarcomere shortening and adrenergic reserve using isoproterenol stimulation (100 nM). CSD reduced cardiac sympathetic activity and prevented IH-induced blunting of cardiomyocyte response to isoproterenol challenge. In hypoxic animals, CSD reduced alterations in long-term ejection fraction and mitigated cardiomyocyte hypertrophy. Transcriptomic analysis unveiled that CSD triggered biological processes related to cardiac repair and regeneration. Immunohistochemistry further supported these findings, demonstrating increased cardiomyocyte proliferation in the hypoxic group, as indicated by elevated Ki67 expression colocalized with MF20 markers. Conclusions Our data demonstrate that cardiac sympathetic denervation prevents IH-induced depletion of cardiac adrenergic reserve and deterioration of cardiac function in a rat model of ischemic cardiomyopathy. This study questions the role of sympathetic activity and hypoxia in cardiac regeneration and on the optimal management of sympathetic hyperactivity in ischemic cardiomyopathy in the specific context of associated SAS.

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Circulating Proteome Profiling Identifies the Hub Proteins and Biological Processes in Ischemic and Non-ischemic Dilated Cardiomyopathy

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