PMID- 12097505
OWN - NLM
STAT- MEDLINE
DCOM- 20020729
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 22
IP  - 13
DP  - 2002 Jul 1
TI  - 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.
PG  - 5536-51
AB  - 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.
FAU - Simpson, P Jeanette
AU  - Simpson PJ
AD  - Departments of Neuroscience and Neurology, The Johns Hopkins University School of 
      Medicine, Baltimore, Maryland 21205, USA.
FAU - Miller, Ian
AU  - Miller I
FAU - Moon, Cheil
AU  - Moon C
FAU - Hanlon, Andrea L
AU  - Hanlon AL
FAU - Liebl, Daniel J
AU  - Liebl DJ
FAU - Ronnett, Gabriele V
AU  - Ronnett GV
LA  - eng
GR  - F32 DC 00406/DC/NIDCD NIH HHS/United States
GR  - R01 NS039657/NS/NINDS NIH HHS/United States
GR  - NS-39657/NS/NINDS NIH HHS/United States
GR  - F32 DC000406/DC/NIDCD NIH HHS/United States
GR  - R01 DC002979/DC/NIDCD NIH HHS/United States
GR  - DC-2979/DC/NIDCD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (guanyl cyclase-B receptor)
RN  - 127869-51-6 (Natriuretic Peptide, C-Type)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - H2D2X058MU (Cyclic GMP)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Brain-Derived Neurotrophic Factor/*antagonists & inhibitors/genetics
MH  - Cell Cycle
MH  - Cell Cycle Proteins/metabolism
MH  - Cell Differentiation/drug effects
MH  - Cell Division/drug effects
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cyclic GMP/physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Mitogen-Activated Protein Kinases/antagonists & inhibitors
MH  - Natriuretic Peptide, C-Type/metabolism/*pharmacology
MH  - Nerve Growth Factor/*antagonists & inhibitors
MH  - Olfactory Pathways/metabolism
MH  - Olfactory Receptor Neurons/*cytology/drug effects/metabolism
MH  - Protein Biosynthesis
MH  - Receptors, Cell Surface/metabolism
MH  - Stem Cells/drug effects/physiology
PMC - PMC6758208
EDAT- 2002/07/05 10:00
MHDA- 2002/07/30 10:01
PMCR- 2003/01/01
CRDT- 2002/07/05 10:00
PHST- 2002/07/05 10:00 [pubmed]
PHST- 2002/07/30 10:01 [medline]
PHST- 2002/07/05 10:00 [entrez]
PHST- 2003/01/01 00:00 [pmc-release]
AID - 22/13/5536 [pii]
AID - 6586 [pii]
AID - 10.1523/JNEUROSCI.22-13-05536.2002 [doi]
PST - ppublish
SO  - J Neurosci. 2002 Jul 1;22(13):5536-51. doi: 10.1523/JNEUROSCI.22-13-05536.2002.