ArticlePloS one2009
BNP signaling is crucial for embryonic stem cell proliferation.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Interventions in the B-type natriuretic peptide signalling pathway as a means of controlling chronic itch.British journal of pharmacology · 2020Review
- Is Atrial Natriuretic Peptide (ANP) and Natriuretic Peptide Receptor-A (NPR-A) Expression in Human Placenta and Decidua Normal?Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Synthesis, secretion, function, metabolism and application of natriuretic peptides in heart failure.Journal of biological engineering · 2018Review
- The multifaceted role of natriuretic peptides in metabolic syndrome.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2017Review
- Natriuretic Peptide Receptor B modulates the proliferation of the cardiac cells expressing the Stem Cell Antigen-1.Scientific reports · 2017Article
- Exogenous Nitric Oxide Protects Human Embryonic Stem Cell-Derived Cardiomyocytes against Ischemia/Reperfusion Injury.Oxidative medicine and cellular longevity · 2016Article
- Localization of Brain Natriuretic Peptide Immunoreactivity in Rat Spinal Cord.Frontiers in neuroanatomy · 2016Article
- Pharmacological Therapy in the Heart as an Alternative to Cellular Therapy: A Place for the Brain Natriuretic Peptide?Stem cells international · 2016Review
- Brain natriuretic peptide constitutively downregulates P2X3 receptors by controlling their phosphorylation state and membrane localization.Molecular pain · 2015Article
- New proteomic insights on the role of NPR-A in regulating self-renewal of embryonic stem cells.Stem cell reviews and reports · 2014Article
- Cytoprotection by the NO-donor SNAP against ischemia/reoxygenation injury in mouse embryonic stem cell-derived cardiomyocytes.Molecular biotechnology · 2014Article
- Molecular mechanisms controlling the cell cycle in embryonic stem cells.Stem cell reviews and reports · 2013Review
- Article
- Stress hormone epinephrine enhances adipogenesis in murine embryonic stem cells by up-regulating the neuropeptide Y system.PloS one · 2012Article
- Proteomic analyses reveal common promiscuous patterns of cell surface proteins on human embryonic stem cells and sperms.PloS one · 2011Article
- NPR-A regulates self-renewal and pluripotency of embryonic stem cells.Cell death & disease · 2011Article
- Oxytocin-Gly-Lys-Arg: a novel cardiomyogenic peptide.PloS one · 2010Article
- Pluripotency maintenance mechanism of embryonic stem cells and reprogramming.International journal of hematology · 2010Review
- Oxytocin: Old Hormone, New Drug.Pharmaceuticals (Basel, Switzerland) · 2009Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEmbryonic stem (ES) cells have unlimited proliferation potential, and can differentiate into several cell types, which represent ideal sources for cell-based therapy. This high-level proliferative ability is attributed to an unusual type of cell cycle. The Signaling pathways that regulate the proliferation of ES cells are of great interest. METHODOLOGY/PRINCIPAL
findingsIn this study, we show that murine ES cells specifically express brain natriuretic peptide (BNP), and its signaling is essential for ES cell proliferation. We found that BNP and its receptor (NPR-A, natriuretic peptide receptor-A) were highly expressed in self-renewing murine ES cells, whereas the levels were markedly reduced after ES cell differentiation by the withdrawal of LIF. Targeting of BNP with short interfering RNA (siRNA) resulted in the inhibition of ES cell proliferation, as indicated by a marked reduction in the cell number and colony size, a significant reduction in DNA synthesis, and decreased numbers of cells in S phase. BNP knockdown in ES cells led to the up-regulation of gamma-aminobutyric acid receptor A (GABA(A)R) genes, and activation of phosphorylated histone (gamma-H2AX), which negatively affects ES cell proliferation. In addition, knockdown of BNP increased the rate of apoptosis and reduced the expression of the transcription factor Ets-1. CONCLUSIONS/SIGNIFICANCE: Appropriate BNP expression is essential for the maintenance of ES cell propagation. These findings establish BNP as a novel endogenous regulator of ES cell 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.