ArticleMolecular and cellular biochemistry2012
Guanylyl cyclase/natriuretic peptide receptor-A signaling antagonizes the vascular endothelial growth factor-stimulated MAPKs and downstream effectors AP-1 and CREB in mouse mesangial cells.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- The role and clinical value of natriuretic peptide receptor family in malignant tumor.Cell death discovery · 2025Review
- The alkylglycerone phosphate synthase sustains the resistance of gastric cancer cells to ferroptosis induced by Apatinib.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025Article
- Guanylyl cyclase/natriuretic peptide receptor-A: Identification, molecular characterization, and physiological genomics.Frontiers in molecular neuroscience · 2022Review
- Protection of kidney function and tissue integrity by pharmacologic use of natriuretic peptides and neprilysin inhibitors.Pflugers Archiv : European journal of physiology · 2021Review
- Molecular Signaling Mechanisms and Function of Natriuretic Peptide Receptor-A in the Pathophysiology of Cardiovascular Homeostasis.Frontiers in physiology · 2021Review
- Depletion of cyclic-GMP levels and inhibition of cGMP-dependent protein kinase activate p21FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Angiotensin II represses Npr1 expression and receptor function by recruitment of transcription factors CREB and HSF-4a and activation of HDACs.Scientific reports · 2020Article
- Emerging concepts of receptor endocytosis and concurrent intracellular signaling: Mechanisms of guanylyl cyclase/natriuretic peptide receptor-A activation and trafficking.Cellular signalling · 2019Review
- Article
- Molecular and genetic aspects of guanylyl cyclase natriuretic peptide receptor-A in regulation of blood pressure and renal function.Physiological genomics · 2018Review
- Clathrin-dependent internalization, signaling, and metabolic processing of guanylyl cyclase/natriuretic peptide receptor-A.Molecular and cellular biochemistry · 2018Article
- Natriuretic peptide receptor guanylyl cyclase-A pathway counteracts glomerular injury evoked by aldosterone through p38 mitogen-activated protein kinase inhibition.Scientific reports · 2017Article
- Zinc-finger protein 418 overexpression protects against cardiac hypertrophy and fibrosis.PloS one · 2017Article
- Plasma levels of natriuretic peptides and development of chronic kidney disease.BMC nephrology · 2015Article
- Subcellular trafficking of guanylyl cyclase/natriuretic peptide receptor-A with concurrent generation of intracellular cGMP.Bioscience reports · 2015Article
- Article
- Guanylyl cyclase/natriuretic peptide receptor-A signaling antagonizes phosphoinositide hydrolysis, Ca(2+) release, and activation of protein kinase C.Frontiers in molecular neuroscience · 2014Review
- Suppression of atrial natriuretic peptide/natriuretic peptide receptor-A-mediated signaling upregulates angiotensin-II-induced collagen synthesis in adult cardiac fibroblasts.Molecular and cellular biochemistry · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Along with its natriuretic, diuretic, and vasodilatory properties, atrial natriuretic peptide (ANP), and its guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) exhibit an inhibitory effect on cell growth and proliferation. However, the signaling pathways mediating this inhibition are not well understood. The objective of this study was to determine the effect of ANP-NPRA system on mitogen-activated protein kinases (MAPKs) and the downstream proliferative transcription factors involving activating protein-1 (AP-1) and cAMP-response element binding protein (CREB) in agonist-stimulated mouse mesangial cells (MMCs). We found that ANP inhibited vascular endothelial growth factor (VEGF)-stimulated phosphorylation of MAPKs (Erk1, Erk2, JNK, and p38), to a greater extent in NPRA-transfected cells (50-60 %) relative to vector-transfected cells (25-30 %). The analyses of the phosphorylated transcription factors revealed that ANP inhibited VEGF-stimulated activation of CREB, and the AP-1 subunits (c-jun and c-fos). Gel shift assays demonstrated that ANP inhibited VEGF-stimulated AP-1 and CREB DNA-binding ability by 67 and 62 %, respectively. The addition of the protein kinase G (PKG) inhibitor, KT-5823, restored the VEGF-stimulated activation of MAPKs, AP-1, and CREB, demonstrating the integral role of cGMP/PKG signaling in NPRA-mediated effects. Our results delineate the underlying mechanisms through which 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.