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Alterations of cardiac protein kinases in cyclic nucleotide-dependent signaling pathways in human ischemic heart failure

ABSTRACT: Alterations of cardiac protein kinases in cyclic nucleotide-dependent signaling pathways in human ischemic heart failure

PROVIDER: PRJNA838927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19241235.fastq.gz	Fastqsanger.gz
	SRR19241236.fastq.gz	Fastqsanger.gz
	SRR19241237.fastq.gz	Fastqsanger.gz
	SRR19241238.fastq.gz	Fastqsanger.gz
	SRR19241239.fastq.gz	Fastqsanger.gz

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Alterations of cardiac protein kinases in cyclic nucleotide-dependent signaling pathways in human ischemic heart failure

Project description:Impaired protein kinase signaling is a hallmark of ischemic heart disease (IHD). Limited treatment options are available due to inadequate understanding of the pathological mechanisms. Identification of the key kinases in the pathogenesis of IHD with an effort to find potential therapeutic strategies is of high importance. Cardiac kinase activity in end-stage human IHD left ventricles (LVs) and the alteration in related signaling pathways were investigated by kinomics, transcriptomics, and proteomics, and by integration of the multi-omics datasets. Protein kinase A (PKA) and protein kinase G (PKG) ranked on top in the activity shift among the cardiac kinases. In the IHD LVs, PKA activity decreased markedly compared with that of controls (62% reduction, p=0.0034) whereas PKG activity remained stable although the amount of PKG protein increased remarkably (65%, p=0.003). mRNA levels of adenylate cyclases (ADCY 1, 3, 5, 9) and cAMP-hydrolysing phosphodiesterases (PDE4A, PDE4D) decreased significantly, while no statistically significant alterations were observed in that of PKGs (PRKG1 and PRKG2) and guanylate cyclases (GUCYs). mRNA level of CNP decreased remarkably whereas those of BNP, ANP and nyprilysin increased significantly in the IHD LVs. Proteomics analysis uncovered a significant reduction in proteins of ‘Energy metabolism’ and ‘Muscle contraction’ in the patients. Multi-omics integration highlighted intracellular signaling by second messengers as the top enriched Reactome pathway. The deficiency in cAMP/PKA signaling pathways is strongly implicated in the pathogenesis of IHD. Natriuretic peptide CNP could be a potential therapeutic target for the modulation of cGMP/PKG signaling.

2022-07-06 | GSE203160 | GEO

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Cardiac gene expression profiling of heart failure treatment with the anti-ischemic drug ranolazine

Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We analyzed whether the anti-ischemic drug ranolazine could retard the progression of heart failure in an experimental model of heart failure induced by 6 months of chronic pressure overload. The study showed that 2 months of ranolazine treatment improved cardiac function of aortic constricted C57BL/6J (B6) mice with symptoms of heart failure as assessed by echocardiography. The microarray gene expression study of heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) untreated 10 month-old C57BL/6J (B6) mice with heart failure induced by 6 months of abdominal aortic constriction (AAC), (ii) 10 month-old B6 mice with 6 months of AAC and two months of treatment with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched, untreated, sham-operated B6 control mice.

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Left ventricular samples from humans with ischemic heart failure and non-failing controls

Project description:LCMS files from tryptic digests of ~1-4 mg piece of heart ventricular tissue from human with ischemic heart failure and non-failing controls. Specimen number correspond to .raw files as follows: Ischemic Heart failure - 54687.1; HF_1_phos.raw 53148.1; HF_2_phos.raw 53589.2; HF_3_phos.raw 54146.1; HF_4_phos.raw 52935.1; HF_5_phos.raw Non-failing - 52941.1; NHF_1_phos.raw 52777.1; NHF_2_phos.raw 53019.2; NHF_3_phos.raw 53058.1; NHF_4_phos.raw 52621.1; NHF_5_phos.raw

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Alterations of Cardiac Protein Kinases in Cyclic Nucleotide-Dependent Signaling Pathways in Human Ischemic Heart Failure.

Project description:ObjectivesImpaired protein kinase signaling is a hallmark of ischemic heart disease (IHD). Inadequate understanding of the pathological mechanisms limits the development of therapeutic approaches. We aimed to identify the key cardiac kinases and signaling pathways in patients with IHD with an effort to discover potential therapeutic strategies.MethodsCardiac kinase activity in IHD left ventricle (LV) and the related signaling pathways were investigated by kinomics, transcriptomics, proteomics, and integrated multi-omics approach.ResultsProtein kinase A (PKA) and protein kinase G (PKG) ranked on top in the activity shift among the cardiac kinases. In the IHD LVs, PKA activity decreased markedly compared with that of controls (62% reduction, p = 0.0034), whereas PKG activity remained stable, although the amount of PKG protein increased remarkably (65%, p = 0.003). mRNA levels of adenylate cyclases (ADCY 1, 3, 5, 9) and cAMP-hydrolysing phosphodiesterases (PDE4A, PDE4D) decreased significantly, although no statistically significant alterations were observed in that of PKGs (PRKG1 and PRKG2) and guanylate cyclases (GUCYs). The gene expression of natriuretic peptide CNP decreased remarkably, whereas those of BNP, ANP, and neprilysin increased significantly in the IHD LVs. Proteomics analysis revealed a significant reduction in protein levels of "Energy metabolism" and "Muscle contraction" in the patients. Multi-omics integration highlighted intracellular signaling by second messengers as the top enriched Reactome pathway.ConclusionThe deficiency in cAMP/PKA signaling pathway is strongly implicated in the pathogenesis of IHD. Natriuretic peptide CNP could be a potential therapeutic target for the modulation of cGMP/PKG signaling.

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Cardiac gene expression profiling of apoE-deficient mice receiving heart failure treatment with the anti-ischemic drug ranolazine

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