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Upregulated Natriuretic Peptide B expression as a hallmark of chronic itch

ABSTRACT: Upregulated Natriuretic Peptide B expression as a hallmark of chronic itch

PROVIDER: PRJNA1247404 | ENA |

REPOSITORIES: ENA

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Upregulated Natriuretic Peptide B expression as a hallmark of chronic itch

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

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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

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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.

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