PMID- 11746354
OWN - NLM
STAT- MEDLINE
DCOM- 20020125
LR  - 20111117
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 66
IP  - 3
DP  - 2001 Nov 1
TI  - Transforming growth factor-beta1 enhances expression of brain-derived 
      neurotrophic factor and its receptor, TrkB, in neurons cultured from rat cerebral 
      cortex.
PG  - 369-76
AB  - The effects of transforming growth factor (TGF)-beta1 on expression of 
      brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, TrkB, in 
      neurons cultured from the cerebral cortex of 18-day-old embryonic rats were 
      examined. BDNF mRNA was significantly increased from 24-48 hr after the TGF-beta1 
      treatment over 20 ng/ml. Accumulation of BDNF protein in the culture medium was 
      also potentiated by TGF-beta1, although the intracellular content of BDNF was 
      nearly unchanged. The enhancement of BDNF mRNA expression was suppressed by the 
      co-presence of decorin, a small TGF-beta-binding proteoglycan that inhibits the 
      biological activities of TGF-betas. mRNA expression of full-length TrkB, the 
      bioactive high-affinity receptor for BDNF, was also upregulated after treatment 
      with TGF-beta1. These observations suggest that: 1) TGF-beta1 potentiates 
      BDNF/TrkB autocrine or local paracrine system; and 2) the neurotrophic activity 
      of TGF-beta1 is partly responsible for the BDNF induced by TGF-beta1 itself. To 
      test this latter possibility, we examined the neuronal survival activity of 
      TGF-beta1 with or without K252a, a selective inhibitor of Trk family tyrosine 
      kinases. TGF-beta1 significantly enhanced neuronal survival, but the co-presence 
      of K252a completely suppressed the activity, demonstrating the involvement of Trk 
      receptor signaling in TGF-beta1-mediated neuronal survival in cultured rat 
      cortical neurons. These results seem to be in line with recent findings by other 
      investigators that some neurotrophic factors including BDNF require TGF-betas as 
      a cofactor to exert their neurotrophic activities.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Sometani, A
AU  - Sometani A
AD  - Laboratory of Molecular Biology, Gifu Pharmaceutical University, Gifu, Japan.
FAU - Kataoka, H
AU  - Kataoka H
FAU - Nitta, A
AU  - Nitta A
FAU - Fukumitsu, H
AU  - Fukumitsu H
FAU - Nomoto, H
AU  - Nomoto H
FAU - Furukawa, S
AU  - Furukawa S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Carbazoles)
RN  - 0 (Dcn protein, rat)
RN  - 0 (Decorin)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (Indole Alkaloids)
RN  - 0 (Proteoglycans)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tgfb1 protein, rat)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 97161-97-2 (staurosporine aglycone)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Autocrine Communication/drug effects/physiology
MH  - Brain-Derived Neurotrophic Factor/drug effects/genetics/*metabolism
MH  - Carbazoles/pharmacology
MH  - Cell Differentiation/drug effects/physiology
MH  - Cell Survival/drug effects/physiology
MH  - Cells, Cultured
MH  - Central Nervous System/cytology/*embryology/metabolism
MH  - Decorin
MH  - Enzyme Inhibitors/pharmacology
MH  - Extracellular Matrix Proteins
MH  - Female
MH  - Fetus
MH  - Gene Expression Regulation, Developmental/drug effects/*physiology
MH  - Indole Alkaloids
MH  - Neurons/cytology/drug effects/*metabolism
MH  - Pregnancy
MH  - Proteoglycans/metabolism/pharmacology
MH  - RNA, Messenger/drug effects/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, trkB/*genetics
MH  - Time Factors
MH  - Transforming Growth Factor beta/*metabolism/pharmacology
MH  - Transforming Growth Factor beta1
MH  - Up-Regulation/drug effects/*physiology
EDAT- 2001/12/18 10:00
MHDA- 2002/01/26 10:01
CRDT- 2001/12/18 10:00
PHST- 2001/12/18 10:00 [pubmed]
PHST- 2002/01/26 10:01 [medline]
PHST- 2001/12/18 10:00 [entrez]
AID - 10.1002/jnr.1229 [pii]
AID - 10.1002/jnr.1229 [doi]
PST - ppublish
SO  - J Neurosci Res. 2001 Nov 1;66(3):369-76. doi: 10.1002/jnr.1229.