ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Atrial natriuretic peptide type C induces a cell-cycle switch from proliferation to differentiation in brain-derived neurotrophic factor- or nerve growth factor-primed olfactory receptor neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- A systematic review of the biological mediators of fat taste and smell.Physiological reviews · 2023Pooled it
- Developmental roles of natriuretic peptides and their receptors.Cells & development · 2023Review
- Olfaction: Sensitive indicator of inflammatory burden in chronic rhinosinusitis.Laryngoscope investigative otolaryngology · 2020Review
- Natriuretic peptide system expression in murine and human submandibular salivary glands: a study of the spatial localisation of ANB, BNP, CNP and their receptors.Journal of molecular histology · 2020Article
- Endothelin increases the proliferation of rat olfactory mucosa cells.Neural regeneration research · 2020Article
- Brain-derived neurotrophic factor: A steroidogenic regulator of Leydig cells.Journal of cellular physiology · 2019Article
- Environmental Enrichment Elicits a Transient Rise of Bioactive C-Type Natriuretic Peptide in Young but Not Aged Rats.Frontiers in behavioral neuroscience · 2018Article
- The Physiology of BDNF and Its Relationship with ADHD.Molecular neurobiology · 2015Review
- Brain-derived neurotrophic factor (Val66Met) polymorphism and olfactory ability in young adults.Journal of biomedical science · 2013Article
- Normal mitral cell dendritic development in the setting of Mecp2 mutation.Neuroscience · 2012Article
- Age-Related Olfactory Decline is Associated with the BDNF Val66met Polymorphism: Evidence from a Population-Based Study.Frontiers in aging neuroscience · 2010Article
- A novel role for jun N-terminal kinase signaling in olfactory sensory neuronal death.Molecular and cellular neurosciences · 2008Article
- ATP7A (Menkes protein) functions in axonal targeting and synaptogenesis.Molecular and cellular neurosciences · 2007Article
- Critical roles of the guanylyl cyclase B receptor in endochondral ossification and development of female reproductive organs.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- VEGF-induced neuroprotection, neurogenesis, and angiogenesis after focal cerebral ischemia.The Journal of clinical investigation · 2003Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
With the discovery of postnatal stem cells within the brain, it has become important to understand how extracellular factors might affect the maturation of neuronal precursors in the postnatal brain. Neurotrophic factors are known to play a role in neuronal development but display pleiotrophic effects, in part because of their physiological interactions with other factors. One factor positioned to interact with neurotrophins in the brains of postnatal animals is atrial C-type natriuretic peptide (CNP). In this study, we used olfactory receptor neurons (ORNs) as a model, because their precursors demonstrate the most robust and functional postnatal neurogenesis of those systems thus far described. We examined the effects of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) and the interactions of these neurotrophins and CNP in postnatal olfactory neuronal precursors. Results obtained using mice with targeted deletion of the gene for BDNF indicated that BDNF is a neuroproliferation-inducing and survival factor for ORN precursors. These roles were confirmed in vitro using primary cultures of ORNs. NGF was found to be a proliferation-inducing factor but not a survival factor. The addition of CNP to either BDNF- or NGF-treated neuronal precursors resulted in an inhibition of proliferation and the promotion of maturation. These effects were accompanied by changes in cell-cycle proteins that suggest possible mechanisms for these effects. Thus, CNP may function in the postnatal brain to regulate the exit from the cell cycle in neuronal precursor cells.
Indexed as
Identifiers
12097505PMC6758208W2134776708What OpenQuestion holds
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.