PMID- 23737642
OWN - NLM
STAT- MEDLINE
DCOM- 20131203
LR  - 20211021
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2013
DP  - 2013
TI  - ATP is required and advances cytokine-induced gap junction formation in microglia 
      in vitro.
PG  - 216402
LID - 10.1155/2013/216402 [doi]
LID - 216402
AB  - Microglia are the immune cells in the central nervous system. After injury 
      microglia release bioactive molecules, including cytokines and ATP, which modify 
      the functional state of hemichannels (HCs) and gap junction channels (GJCs), 
      affecting the intercellular communication via extracellular and intracellular 
      compartments, respectively. Here, we studied the role of extracellular ATP and 
      several cytokines as modulators of the functional state of microglial HCs and 
      GJCs using dye uptake and dye coupling techniques, respectively. In microglia and 
      the microglia cell line EOC20, ATP advanced the TNF-alpha/IFN-gamma-induced dye coupling, 
      probably through the induction of IL-1beta release. Moreover, TNF-alpha/IFN-gamma, but not 
      TNF-alpha plus ATP, increased dye uptake in EOC20 cells. Blockade of Cx43 and Panx1 
      HCs prevented dye coupling induced by TNF-alpha/IFN-gamma, but not TNF-alpha plus ATP. In 
      addition, IL-6 prevented the induction of dye coupling and HC activity induced by 
      TNF-alpha/IFN-gamma in EOC20 cells. Our data support the notion that extracellular ATP 
      affects the cellular communication between microglia through autocrine and 
      paracrine mechanisms, which might affect the timing of immune response under 
      neuroinflammatory conditions.
FAU - Saez, Pablo J
AU  - Saez PJ
AD  - Departamento de Fisiologia, Pontificia Universidad Catolica de Chile, Alameda 
      340, 6513677 Santiago, Chile. pjsaez@uc.cl
FAU - Shoji, Kenji F
AU  - Shoji KF
FAU - Retamal, Mauricio A
AU  - Retamal MA
FAU - Harcha, Paloma A
AU  - Harcha PA
FAU - Ramirez, Gigliola
AU  - Ramirez G
FAU - Jiang, Jean X
AU  - Jiang JX
FAU - von Bernhardi, Rommy
AU  - von Bernhardi R
FAU - Saez, Juan C
AU  - Saez JC
LA  - eng
GR  - R01 EY012085/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130423
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Adenosine Triphosphate
MH  - Animals
MH  - Blotting, Western
MH  - Cell Line
MH  - Cells, Cultured
MH  - Cytokines/*pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fluorescent Antibody Technique
MH  - Gap Junctions/*metabolism
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-1beta/pharmacology
MH  - Interleukin-6/pharmacology
MH  - Mice
MH  - Microglia/cytology/*drug effects/*metabolism
MH  - Rats
MH  - Tumor Necrosis Factor-alpha/pharmacology
PMC - PMC3655668
EDAT- 2013/06/06 06:00
MHDA- 2013/12/16 06:00
PMCR- 2013/04/23
CRDT- 2013/06/06 06:00
PHST- 2013/02/04 00:00 [received]
PHST- 2013/03/21 00:00 [revised]
PHST- 2013/03/22 00:00 [accepted]
PHST- 2013/06/06 06:00 [entrez]
PHST- 2013/06/06 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
PHST- 2013/04/23 00:00 [pmc-release]
AID - 10.1155/2013/216402 [doi]
PST - ppublish
SO  - Mediators Inflamm. 2013;2013:216402. doi: 10.1155/2013/216402. Epub 2013 Apr 23.