PMID- 10220111
OWN - NLM
STAT- MEDLINE
DCOM- 19990610
LR  - 20161124
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 55
IP  - 6
DP  - 1999 Mar 15
TI  - Phosphorylation of CREB in axon-induced Schwann cell proliferation.
PG  - 702-12
AB  - Axonal contact regulates Schwann cell (SC) proliferation during development.
      However, the intracellular signal transduction pathways involved in the
      axon-induced proliferation of SC have not been described. We have previously
      shown that SC proliferation induced by axolemma-enriched fractions (AEF) is
      accompanied by increased expression of cyclic AMP-responsive element binding
      protein, CREB. We now report the AEF and dorsal root ganglion neuritic-induced
      signal transduction pathway(s) which regulate the phosphorylation of CREB that
      correlate with the SC proliferative response. The phosphorylated form of CREB was
      significantly increased after 16 hr of axonal stimulation, continued to increase 
      for 48 hr, and subsequently decreased as monitored by immunocytochemistry and
      Western blot analysis. Treatment with protein kinase A (PKA) inhibitor, H89,
      completely abolished both the CREB activation and SC proliferation. In contrast, 
      treatment with protein kinase C (PKC) inhibitor (bisindolylmaleimide) inhibited
      AEF-induced SC proliferation, but did not immediately affect CREB
      phosphorylation. These data are consistent with the view that PKA and PKC
      pathways are essential for AEF-induced SC proliferation. Since PKC can influence 
      SC proliferation without initially affecting CREB phosphorylation, PKC may
      regulate SC proliferation at pathways distal to the immediate CREB activation.
FAU - Lee, M M
AU  - Lee MM
AD  - Mental Retardation Research Center, Department of Neurobiology, University of
      California School of Medicine, Los Angeles, USA.
FAU - Badache, A
AU  - Badache A
FAU - DeVries, G H
AU  - DeVries GH
LA  - eng
GR  - NINDS 15408/DS/DS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Indoles)
RN  - 0 (Isoquinolines)
RN  - 0 (Maleimides)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Sulfonamides)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - M876330O56 (N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide)
RN  - MBK3OO5K8T (bisindolylmaleimide)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Axons/*physiology
MH  - Cell Division
MH  - Cells, Cultured
MH  - Cyclic AMP Response Element-Binding Protein/*metabolism
MH  - Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/*metabolism
MH  - Embryo, Mammalian
MH  - Enzyme Inhibitors/pharmacology
MH  - Ganglia, Spinal/cytology/*physiology
MH  - Indoles/pharmacology
MH  - Isoquinolines/pharmacology
MH  - Kinetics
MH  - Maleimides/pharmacology
MH  - Neurites/physiology
MH  - Nuclear Proteins/metabolism
MH  - Phosphorylation
MH  - Protein Kinase C/antagonists & inhibitors
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Schwann Cells/*cytology/*physiology
MH  - Sciatic Nerve/cytology/*physiology
MH  - Signal Transduction
MH  - *Sulfonamides
MH  - Time Factors
EDAT- 1999/04/29 02:03
MHDA- 2000/06/20 09:00
CRDT- 1999/04/29 02:03
PHST- 1999/04/29 02:03 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/04/29 02:03 [entrez]
AID - 10.1002/(SICI)1097-4547(19990315)55:6<702::AID-JNR5>3.0.CO;2-N [pii]
AID - 10.1002/(SICI)1097-4547(19990315)55:6<702::AID-JNR5>3.0.CO;2-N [doi]
PST - ppublish
SO  - J Neurosci Res. 1999 Mar 15;55(6):702-12. doi:
      10.1002/(SICI)1097-4547(19990315)55:6<702::AID-JNR5>3.0.CO;2-N.