PMID- 19048368
OWN - NLM
STAT- MEDLINE
DCOM- 20090706
LR  - 20211020
IS  - 1573-6830 (Electronic)
IS  - 0272-4340 (Linking)
VI  - 29
IP  - 3
DP  - 2009 May
TI  - MCP-1-induced migration of NT2 neuroprogenitor cells involving APP signaling.
PG  - 373-81
LID - 10.1007/s10571-008-9329-3 [doi]
AB  - Neuroprogenitor cells are an important resource because of their great potential 
      to replace damaged cells in the brain caused by trauma and disease. Studies have 
      shown that when neuroprogenitor cells are transplanted into the brain they 
      migrate towards damaged areas, suggesting that these areas express factors that 
      recruit migrating cells. Generally, after neuronal injury, there is a 
      neuroinflammatory response that results in increased chemokine production. In 
      this present study, we demonstrate that monocyte chemoattractant protein-1 
      (MCP-1) significantly induces the migration of NT2 neuroprogenitor cells. 
      Activation of intracellular cyclic adenosine monophosphate or protein kinase C 
      with forskolin and phorbol 12-myristate 13-acetate, respectively, was able to 
      completely abolish the MCP-1-induced migration. Contrarily, neither extracellular 
      signal-regulated kinase nor p38 mitogen-activated protein kinase was required for 
      NT2 cells to respond to MCP-1. Previously, we showed that amyloid precursor 
      protein (APP) activity increases MCP-1 expression in NT2 cells. We now 
      demonstrate that NT2 cells expressing APP can induce migration of other 
      neuroprogenitor cells. Utilizing a MCP-1 neutralizing antibody, we discovered 
      that APP-induced migration was not caused solely by increased MCP-1 production. 
      Interestingly, APP-increased expression of several C-C chemokines: MCP-1, 
      regulated upon activation, normal T-cell expressed, and secreted (RANTES), and 
      macrophage inflammatory protein alpha (MIP-1 alpha). This demonstrates the unique 
      role APP has in regulating chemokine production, which directly affects cell 
      migration. Taken together, these data provides greater detail of the chemotactic 
      factors and intracellular signaling that direct neuroprogenitor cell migration, 
      allowing for better understanding of cell migration during transplantation.
FAU - Vrotsos, Emmanuel George
AU  - Vrotsos EG
AD  - Burnett School of Biomedical Sciences, College of Medicine, University of Central 
      Florida, 4000 Central Florida Blvd. BMS Building, Room 223, Orlando, FL 
      32816-2364, USA.
FAU - Sugaya, Kiminobu
AU  - Sugaya K
LA  - eng
PT  - Journal Article
DEP - 20081202
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Amyloid beta-Protein Precursor/*metabolism
MH  - Cell Line, Tumor
MH  - Cell Movement/*drug effects
MH  - Chemokine CCL2/*pharmacology
MH  - Chemotaxis/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Neurons/*cytology/drug effects
MH  - Neutralization Tests
MH  - RNA, Messenger/genetics/metabolism
MH  - Signal Transduction/*drug effects
MH  - Stem Cells/*cytology/drug effects
MH  - Time Factors
MH  - Transfection
EDAT- 2008/12/03 09:00
MHDA- 2009/07/07 09:00
CRDT- 2008/12/03 09:00
PHST- 2008/09/16 00:00 [received]
PHST- 2008/11/06 00:00 [accepted]
PHST- 2008/12/03 09:00 [pubmed]
PHST- 2009/07/07 09:00 [medline]
PHST- 2008/12/03 09:00 [entrez]
AID - 10.1007/s10571-008-9329-3 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2009 May;29(3):373-81. doi: 10.1007/s10571-008-9329-3. Epub 
      2008 Dec 2.