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Endogenous ANP/guanylyl cyclase-A signaling improves the initial adaptative response of beta-cells to high fat diet-induced obesity. Impaired beta-cell ANP/GC-A signaling in obese individuals might contribute to the development of type 2 diabetes.
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A decreased Npr1 copy number enhanced the expression of hypertrophic markers.
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The results indicate that the inhibition of NPRA suppresses gastric cancer development and targeting NPRA may represent a promising strategy for the treatment of gastric cancer.
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KLF10 and atrial natriuretic peptide/NPRA in exerting influences on chronic pulmonary disease pathogenesis
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Treatment of the haplotype Npr1(+/-) mice with histone deacetylase inhibitors significantly lowered blood pressure and reduced the renal inflammation and fibrosis involving the interactive roles of HDAC1/2, NF-kappaB (p65), and STAT1.
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Data suggest that the negative inhibition of P2X3R activity by the BNP/NPR-A pathway results in a decreased P2X3R-mediated excitability of trigeminal neurons in wildetype cultures. In familial hemiplegic migraine type-1 model cultures, however, lack of efficient P2X3Rs downregulation contributes to the neuronal hyperexcitability phenotype.
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The results suggest that an antagonistic cascade exists between the TGF-beta1/Smad/deltaEF1 pathways and Npr1 expression and receptor signaling that is relevant to renal and vascular remodeling, and may be critical in the regulation of blood pressure and cardiovascular homeostasis.
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Conclude that postnatal cardiac hyperplasia in mice with global GC-A inactivation is provoked by systemic alterations rather than direct regulation of cardiac myocyte proliferation.
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Data (including data from studies in knockout mice) suggest expression of ANP/BNP/GC-A (atrial natriuretic peptide, brain natriuretic peptide, and guanylyl cyclase-A) is important in embryonic neovascularization and organogenesis.
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Suggest that the FQQI motif is essential for the internalization and subcellular trafficking of NPRA during the hormone signaling process in intact mesangial cells.
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Data suggest activation of skeletal muscle (SM) Npra is important for maintenance of long-term insulin sensitivity; up-regulation of Npra signal transduction in SM (that was reduced by obesity) prevents glucose intolerance and diabetes type 2.
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these findings define a novel epigenetic regulatory mechanism that governs Npr1 gene transcription.
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Npr1 represses the expression of cardiac proinflammatory mediators, hypertrophic markers, and NF-kappaB/AP-1-mediated mechanisms, which seem to be associated in an Npr1 gene-dose-dependent manner
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ANP is capable of attenuating agonist-induced lung edema in the absence of NPR-A.
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These results demonstrate that a high-salt diet aggravates cardiac ANG II, aldosterone and pro-inflammatory cytokine levels in Npr1 gene-disrupted 1-copy mice, whereas, in Npr1 gene-duplicated (3-copy and 4-copy) mice, high salt did not render such elevation, suggesting the potential roles of Npr1 against salt loading.
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ANP-NPRA system exerts an inhibitory effect on MAPKs and down-stream effector molecules, AP-1, and CREB, critical for cell growth and proliferation.
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Natriuretic peptide receptor guanylyl cyclase-A protects podocytes from aldosterone-induced glomerular injury.
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The consequences of the disruption of Npr1 gene on proinflammatory responses of nuclear factor kappa B, inhibitory kappa B kinase, and inhibitory kappa B alpha (NF-kappaB, IKK, IkappaBalpha) in the kidneys of mutant mice, was determined.
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Results demonstrate the opposite effects of NPR-A and NPR-C in LPS-mediated endothelial permeability and lung injury.
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Data suggest that a NPPA gradient originating in the oviduct induces sperm chemotaxis by binding to its receptor NPR1 and then activating PKG pathway, and plays a physiological role in fertilization.
