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• W1906216417 abstract "Background: Natriuretic peptides ProANP and Pro BNP are translated as biologically-inactive pro-hormones that require proteolytic cleavage into biologically active carboxyl-terminal fragments by the serine protease Corin. Activated ANP and BNP bind to GC-A or natriuretic peptide receptor A (NPRA), which increases intracellular second messenger cGMP, and further stimulates three known cGMP effector molecules: cGMP-dependent protein kinases (PKGs), cGMP-dependent phosphodiesterases (PDEs), and cGMP-dependent ion channels. This produces anti-hypertension, anti-hypertrophy and anti-fibrosis effects. The two linked SNP mutations in Corin gene are associated with risk for hypertension and left-ventricular hypertrophy in Blacks. Novel drugs are needed to target this pathway to improve cardiac functions that impaired by the genetic defects and complications caused by many types of heart failure. Methods and Results: We tested a NPR-A agonist PL3994, synthetic molecule made by Palatin Pharmaceutical Company for its potential therapeutic effects on heart failure and cardiac defects. By using our unique Tamoxifen inducible Corin cardiac specific knockout mouse model and Corin T623I/Q636P knockin mouse model, we implant osmotic pumps with PL3994 or PBS into the mice for four weeks while simultaneously constricted mouse aorta artery by TAC by microsurgery. We recorded cardiac function changes by blood pressure, ECHO, and at end stage measured gene expression profiles, hypertrophy, fibrosis and natriuretic pathway molecule: cGMP, cGMP dependent kinases, ANP28/ProANP128, BNP45/proBNP95 in the explanted hearts and plasma. Results. As compared to WT controls, Corin knockout mice and Corin T623I/Q636P knockin mice showed much worse cardiac hypertrophy by ECHO and heart weight and much worse cardiac fibrosis by Trichrome staining. These phenotypes are also supported by the evidences of less signaling cGMP, less PKG kinase activity in the Corin knockout and knockin mice. However, compared to placebo PBS saline, NPR-A agonist PL3994 significantly improved cardiac conditions with less cardiac hypertrophy and fibrosis, also together with increased signaling cGMP, less PKG kinase activity. Conclusions: NPR-A agonist PL3994 is a potential therapeutic drug to treat patients with Corin genetic defects and patients of heart failure caused by malfunctions of natriuretic pathways." @default.
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• W1906216417 date "2015-08-01" @default.
• W1906216417 modified "2023-09-28" @default.
• W1906216417 title "Paroxetine-Mediated GRK2 Inhibition Reverses Cardiac Dysfunction and Remodeling After Myocardial Infarction" @default.
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• W1906216417 doi "https://doi.org/10.1016/j.cardfail.2015.06.318" @default.
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