PMID- 19357131
OWN - NLM
STAT- MEDLINE
DCOM- 20111220
LR  - 20211020
IS  - 1741-7899 (Electronic)
IS  - 1470-1626 (Print)
IS  - 1470-1626 (Linking)
VI  - 138
IP  - 1
DP  - 2009 Jul
TI  - NTRK1 and NTRK2 receptors facilitate follicle assembly and early follicular 
      development in the mouse ovary.
PG  - 131-40
LID - 10.1530/REP-08-0474 [doi]
AB  - Recent studies have demonstrated that neurotrophins (NTs) and their NTRK tyrosine 
      kinase receptors, thought to be exclusively required for the development of the 
      nervous system, are also involved in controlling ovarian development. Here, we 
      show that primordial follicle formation is decreased in the absence of nerve 
      growth factor (NGF) or its receptor NTRK1, and in the absence of NTRK2, the 
      receptor for neurotrophin-4 (NTF4) and brain-derived neurotrophic factor (BDNF). 
      This deficiency is not due to premature oocyte loss, because the ovaries of 
      Ntrk1(-/-) and Ntrk2(-/-) mice do not show an increased rate of oocyte death 
      antedating the initiation of folliculogenesis. Moreover, exposure of 
      NGF-deficient ovaries to NGF rescues the defect in follicular assembly, if NTRK1 
      receptors are present, suggesting that the absence of NTs causes a delay, and not 
      an irretrievable loss, of follicle formation. Both the number of secondary 
      follicles and FSH receptor (FSHR) expression are diminished in Ntrk1- and 
      Ntrk2-null ovaries, but not in ovaries lacking the common NT receptor NGFR. 
      Transient exposure of wild-type ovaries to NTF4 increases Fshr gene expression 
      and enhances the ability of the ovary to respond to FSH with formation of cyclin 
      D2, a cell cycle protein mediating the proliferative actions of FSH in the ovary. 
      These results indicate that both NTRK1 and NTRK2 receptors are necessary for the 
      timely assembly of primordial follicles and for sustaining early follicular 
      development. They also suggest that a mechanism by which NTRK2 receptors 
      facilitate subsequent follicle development is by inducing the formation of 
      functional FSHR.
FAU - Kerr, Bredford
AU  - Kerr B
AD  - Division of Neuroscience, Oregon National Primate Research Center/Oregon Health 
      and Science University, 505 Northwest 185th Avenue, Beaverton, Oregon 97006, USA.
FAU - Garcia-Rudaz, Cecilia
AU  - Garcia-Rudaz C
FAU - Dorfman, Mauricio
AU  - Dorfman M
FAU - Paredes, Alfonso
AU  - Paredes A
FAU - Ojeda, Sergio R
AU  - Ojeda SR
LA  - eng
GR  - HD18185/HD/NICHD NIH HHS/United States
GR  - P51 RR000163/RR/NCRR NIH HHS/United States
GR  - D43 TW000668/TW/FIC NIH HHS/United States
GR  - HD24870/HD/NICHD NIH HHS/United States
GR  - K01 RR000163/RR/NCRR NIH HHS/United States
GR  - R01 HD024870-20/HD/NICHD NIH HHS/United States
GR  - P51 RR000163-49/RR/NCRR NIH HHS/United States
GR  - P30 HD018185/HD/NICHD NIH HHS/United States
GR  - HD00668/HD/NICHD NIH HHS/United States
GR  - U54 HD018185-25/HD/NICHD NIH HHS/United States
GR  - R01 HD024870/HD/NICHD NIH HHS/United States
GR  - U54 HD018185/HD/NICHD NIH HHS/United States
GR  - D43 TW000668-13/TW/FIC NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20090408
PL  - England
TA  - Reproduction
JT  - Reproduction (Cambridge, England)
JID - 100966036
RN  - 0 (Ccnd2 protein, mouse)
RN  - 0 (Cyclin D2)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Receptors, FSH)
RN  - 9002-68-0 (Follicle Stimulating Hormone)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (Ntrk2 protein, mouse)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis
MH  - Cyclin D2/metabolism
MH  - Female
MH  - Follicle Stimulating Hormone/metabolism
MH  - Membrane Glycoproteins/deficiency/genetics/*metabolism
MH  - Mice
MH  - Mice, 129 Strain
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Nerve Growth Factor/deficiency/genetics
MH  - Nerve Growth Factors/metabolism
MH  - Oocytes/*metabolism/pathology
MH  - Ovarian Follicle/*metabolism/pathology
MH  - Ovary/*metabolism/pathology
MH  - Protein-Tyrosine Kinases/deficiency/genetics/*metabolism
MH  - Receptor, trkA/deficiency/genetics/*metabolism
MH  - Receptors, FSH/metabolism
MH  - Signal Transduction
MH  - Time Factors
MH  - Tissue Culture Techniques
PMC - PMC3150184
MID - NIHMS110155
EDAT- 2009/04/10 09:00
MHDA- 2011/12/21 06:00
PMCR- 2011/08/04
CRDT- 2009/04/10 09:00
PHST- 2009/04/10 09:00 [entrez]
PHST- 2009/04/10 09:00 [pubmed]
PHST- 2011/12/21 06:00 [medline]
PHST- 2011/08/04 00:00 [pmc-release]
AID - REP-08-0474 [pii]
AID - 10.1530/REP-08-0474 [doi]
PST - ppublish
SO  - Reproduction. 2009 Jul;138(1):131-40. doi: 10.1530/REP-08-0474. Epub 2009 Apr 8.