PMID- 21162127
OWN - NLM
STAT- MEDLINE
DCOM- 20110408
LR  - 20220223
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 89
IP  - 2
DP  - 2011 Feb
TI  - Expression of macrophage inflammatory protein-1alpha and monocyte chemoattractant 
      protein-1 in glioma-infiltrating microglia: involvement of ATP and P2X(7) receptor.
PG  - 199-211
LID - 10.1002/jnr.22538 [doi]
AB  - Chemokines can be produced by gliomas, which mediate the infiltration of 
      microglia, a characteristic feature of glioma-associated neuropathogenesis. ATP 
      that is released at a high level from glioma has been reported to play a 
      regulatory role in chemokine production in cultured glioma cells. The objective 
      of this study was to define the potential role of extracellular ATP in the 
      regulation of macrophage inflammatory protein-1alpha (MIP-1alpha) and monocyte 
      chemoattractant protein-1(MCP-1) expression in glioma-associated 
      microglia/macrophages. The results showed that Iba1(+) and ED1(+) microglia 
      existed in the tumor at 3 and 7 day after injection of C6 glioma cells into the 
      rat cerebral cortex (dpi). ED1(+) microglia/macrophages or Iba1(+) microglia in 
      the glioma were also colocalized to MIP-1alpha- and MCP-1-expressing cells. In vitro 
      study indicated that treatment with ATP and BzATP (an agonist for ATP ionotropic 
      receptor P2X(7)R) caused an increase in the intracellular levels of microglial 
      MIP-1alpha and MCP-1. By using an extracellular Ca(2+) chelator (EGTA) and P2X(7)R 
      antagonists, oxidized ATP (oxATP) and brilliant blue G (BBG), we demonstrated 
      that BzATP-induced production of MIP-1alpha and MCP-1 levels was due to P2X(7)R 
      activation and Ca(2+) -dependent regulation. Coadministration of C6 glioma cells 
      and oxATP into the rat cerebral cortex resulted in a reduction of MIP-1alpha- and 
      MCP-1-expressing microglia/macrophages. We suggest, based on the results from in 
      vivo and in vitro studies, that a massive amount of ATP molecules released in the 
      glioma tumor site may act as the regulator with P2X(7)R signaling that increases 
      MIP-1alpha and MCP-1 expression in tumor-infiltrating microglia/macrophages.
CI  - Copyright (c) 2010 Wiley-Liss, Inc.
FAU - Fang, Kuan-Min
AU  - Fang KM
AD  - Department of Life Sciences, National Cheng Kung University, Tainan, Taiwan.
FAU - Wang, Ying-Lan
AU  - Wang YL
FAU - Huang, Ming-Chao
AU  - Huang MC
FAU - Sun, Synthia H
AU  - Sun SH
FAU - Cheng, Henrich
AU  - Cheng H
FAU - Tzeng, Shun-Fen
AU  - Tzeng SF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101208
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Receptors, Purinergic P2X)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Adenosine Triphosphate/*metabolism
MH  - Animals
MH  - Cell Line, Tumor
MH  - Chemokine CCL2/*biosynthesis
MH  - Chemokine CCL3/*biosynthesis
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Fluorescent Antibody Technique
MH  - Gene Expression
MH  - Gene Expression Regulation
MH  - Glioma/immunology/*metabolism
MH  - Immunohistochemistry
MH  - Microglia/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Purinergic P2X/*metabolism
EDAT- 2010/12/17 06:00
MHDA- 2011/04/09 06:00
CRDT- 2010/12/17 06:00
PHST- 2010/05/31 00:00 [received]
PHST- 2010/09/21 00:00 [revised]
PHST- 2010/09/27 00:00 [accepted]
PHST- 2010/12/17 06:00 [entrez]
PHST- 2010/12/17 06:00 [pubmed]
PHST- 2011/04/09 06:00 [medline]
AID - 10.1002/jnr.22538 [doi]
PST - ppublish
SO  - J Neurosci Res. 2011 Feb;89(2):199-211. doi: 10.1002/jnr.22538. Epub 2010 Dec 8.