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Cardiac specific deletion of natriuretic peptide receptor A induces different myocardial expression of circular RNA and mRNA involved with metabolism in mice

ABSTRACT: Cardiac specific deletion of natriuretic peptide receptor A induces different myocardial expression of circular RNA and mRNA involved with metabolism in mice

PROVIDER: PRJNA590497 | ENA |

REPOSITORIES: ENA

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Cardiac specific deletion of natriuretic peptide receptor A induces different myocardial expression of circular RNA and mRNA involved with metabolism in mice

Project description:Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are not only important biological markers, but also regulators of cardiac functions. The natriuretic peptide A receptor (NPRA), also called NPR1 or guanylyl cyclase A (GC-A), binds with ANP or BNP ligand and fulfils transmembrane signalling transduction by elevating the intracellular levels of cGMP. However, the comprehensive effects and mechanisms downstream to NPRA are still largely to be elucidated. Here, the cardiac expressing profiles of mRNA in the mice with myocardium-specific deletion of NPRA were analyzed. It was found that differently expressed mRNAs were detected and proved by Gene Ontology (GO) and pathway analysis to be mainly related to the metabolic process. Moreover, circular RNAs (circRNAs) were scrutinized, and subsequently a possible regulatory network consisting of circRNAs- MicroRNAs (miRNAs) -mRNAs was predicted and constructed by ceRNA (competing endogenous RNA) analysis. In conclusion, NPRA plays possible roles in cardiac metabolism, which might be mediated by circRNAs via endogenous competition mechanisms.

2020-12-08 | GSE140678 | GEO

Impairment of cardiac natriuretic peptide signaling develops the excessive cardiac hypertrophy during lactation period

Project description:Two natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) act through the common receptor, guanylyl cyclase-A (GC-A) to lower blood pressure, induce diuresis/natriuresis and dilate blood vessels. Recently, we discovered that the excessive cardiac hypertrophy accompanied with cardiac dysfunction was induced in the lactating natriuretic peptide receptor 1 (Npr1, which encodes GC-A)-deficient mice. To clarify the cause of lactation-induced cardic hypertrophy in Npr1-/-, we performed the gene expressions analysis using nulliparous (NP) or postpartum lactating wild-type (Npr1+/+) and Npr1-/- mice. Numerous genes were altered in the postpartum lactating period both in Npr1+/+ and Npr1-/-. Additionally, the involvement of inflammatory responce in the cardiac hypertrophy in lactating-Npr1-/- mice was clarified bythe gene ontology analysis.

2019-09-01 | GSE84744 | GEO

Natriuretic Peptide Receptor 3 (NPR3) is regulated by microRNA-100

Project description:The cardiac natriuretic peptide (NPs) plays an important role in the regulation of cardiovascular and renal function. We examined the miRNAs that could be regulating NPs by subjecting the cardiomyocytes, HCMa cells, to hypoxia.

2015-03-23 | GSE55387 | GEO

Beige Fat, Energy, and the Natriuretic Peptide System

Project description:Beige Fat, Energy, and the Natriuretic Peptide System

| PRJNA1065008 | ENA

Beige Fat, Energy, and the Natriuretic Peptide System

Project description:The purpose of this study is to learn how types of fat profiles differ between lean and obese individuals, and how they differ between racial groups. We are also interested in learning about the relationship of fat profiles with natriuretic peptide hormones, which are hormones produced by the heart. We will measure this by collecting tissue, blood and urine samples, energy expenditure measurements using the metabolic cart, and a DXA to assess the amount of bone, fat and muscle in the body from a single study visit.

2024-10-24 | GSE253305 | GEO

Cardiac?specific deletion of natriuretic peptide receptor A induces differential myocardial expression of circular RNA and mRNA molecules involved in metabolism in mice.

Project description:Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are important biological markers and regulators of cardiac function. The natriuretic peptide receptor A (NPRA), also known as NPR1 or guanylyl cyclase A, binds ANP and BNP to initiate transmembrane signal transduction by elevating the intracellular levels of cyclic guanosine monophosphate. However, the effects and mechanisms downstream of NPRA are largely unknown. The aim of the present study was to evaluate the changes in the global pattern of mRNA and circular RNA (circRNA) expression in NPRA?/? and NPRA+/+ myocardium. Differentially expressed mRNA molecules were characterised using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis and were found to be primarily related to metabolic processes. Moreover, circRNA expression was also examined, and a possible competing endogenous RNA network consisting of circRNA, microRNA (miRNA), and mRNA molecules was constructed. The results of this study indicated that NPRA may play a role in cardiac metabolism, which could be mediated by circRNA through endogenous competition mechanisms. These findings may provide insight into future characterisation of various ceRNA network pathways.

| S-EPMC7706000 | biostudies-literature

Identification of natriuretic peptide receptor A (NPR-A) expression signatures in podocytes in vivo reveals baseline control of protective pathways including Protein S

Project description:Natriuretic peptide receptor-A (NPR-A) is the principal receptor for the natriuretic peptides ANP and BNP. Targeted deletion of NPR-A in mouse glomerular podocytes significantly enhances renal injury in vivo in the DOCA-salt experimental model. It was therefore hypothesized that natriuretic peptides exert a direct protective effect on glomerular barrier integrity through activation of NPR-A and modulation of gene expression patterns in podocytes. RNA-seq analysis revealed a total of 158 DEGs with 81 downregulated DEGs and 77 upregulated DEGs in Npr1 deficient podocytes. Among the downregulated genes were protein S and semaphorin 3G, which are known to have a protective effect in podocytes. Protein S was also expressed in and secreted from isolated human glomeruli. GO enrichment analysis revealed that the upregulated DEGs in NPR-A deficient podocytes were associated with cell migration and motility. In line, BNP significantly decreased podocyte outgrowth from cultured glomeruli.

2024-10-02 | GSE249221 | GEO

Inhibition of Fap Promotes Cardiac Repair by Stabilizing BNP

Project description:Inhibition of fibroblast activation protein promotes cardiac repair by stabilizing brain natriuretic peptide after myocardial infarction

2023-01-26 | GSE184986 | GEO

Modified C-type natriuretic peptide normalizes tumor vasculature and improves solid tumor therapies

Project description:Modified C-type natriuretic peptide normalizes tumor vasculature and improves solid tumor therapies

| PRJNA1016266 | ENA

Modified C-type natriuretic peptide normalizes tumor vasculature and improves solid tumor therapies

Project description:Deficit of oxygen and nutrients in the tumor microenvironment (TME) triggers abnormal angiogenesis that produces dysfunctional and leaky blood vessels, which fail to adequately perfuse tumor tissues. Resulting hypoxia, exacerbation of metabolic problems and generation of immunosuppressive TME undermine the efficacy of cancer treatment. These problems can be partially alleviated by angiogenesis inhibitors. Here we propose an alternative agonist-based normalization approach utilizing a derivative of the C-type natriuretic peptide (dCNP). This well-tolerated agent stimulated formation of highly functional tumor blood vessels to reduce hypoxia. Administration of dCNP also inhibited stromagenesis and reinvigorated the anti-tumor immune responses. Treatment with dCNP decelerated growth of primary tumors and suppressed their metastases. Moreover, inclusion of dCNP into the chemo-, radio- or immune-therapeutic regimens increased their efficacy against solid tumors. These results demonstrate the proof of principle for using activators of normalized angiogenesis to improve therapies against solid tumors and characterize dCNP as the first in class amongst such agents.

2023-10-16 | GSE243040 | GEO

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