PMID- 12112372
OWN - NLM
STAT- MEDLINE
DCOM- 20020823
LR  - 20071115
IS  - 0894-1491 (Print)
IS  - 0894-1491 (Linking)
VI  - 39
IP  - 1
DP  - 2002 Jul
TI  - RANTES stimulates inflammatory cascades and receptor modulation in murine 
      astrocytes.
PG  - 19-30
AB  - Cultured mouse astrocytes respond to the CC chemokine RANTES by production of 
      chemokine and cytokine transcripts. Stimulation of astrocytes with 1 nM RANTES or 
      3-10 nM of the structurally related chemokines (eotaxin, macrophage inflammatory 
      protein-1alpha and -beta [MIP-1alpha, MIP-1beta]) induced transcripts for KC, 
      monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha 
      (TNF-alpha), MIP-1alpha, MIP-2, and RANTES in a chemokine and cell-specific 
      fashion. Synthesis of chemokine (KC and MCP-1) and cytokine (TNF-alpha) proteins 
      was also demonstrated. RANTES-mediated chemokine synthesis was specifically 
      inhibited by pertussis toxin, indicating that G-protein-coupled chemokine 
      receptors participated in astrocyte signaling. Astrocytes expressed CCR1 and CCR5 
      (the redundant RANTES receptors). Astrocytes derived from mice with targeted 
      mutations of either CCR1 or CCR5 respond after RANTES stimulation, suggesting 
      multiple chemokine receptors may separately mediate RANTES responsiveness in 
      astrocytes. Preliminary data suggest activation of the MAP kinase pathway is also 
      critical for RANTES-mediated signaling in astrocytes. Treatment with RANTES 
      specifically modulated astrocyte receptors upregulating intercellular adhesion 
      molecule 1 (ICAM-1) and downregulating CX3CR1 expression. Thus, after chemokine 
      treatment, astrocytes release proinflammatory mediators and reprogram their 
      surface molecules. The combined effects of RANTES may serve to amplify 
      inflammatory responses within the central nervous system.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Luo, Yi
AU  - Luo Y
AD  - Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, 
      USA.
FAU - Berman, Michael A
AU  - Berman MA
FAU - Zhai, Qiwei
AU  - Zhai Q
FAU - Fischer, Falko R
AU  - Fischer FR
FAU - Abromson-Leeman, Sara R
AU  - Abromson-Leeman SR
FAU - Zhang, Ye
AU  - Zhang Y
FAU - Kuziel, William A
AU  - Kuziel WA
FAU - Gerard, Craig
AU  - Gerard C
FAU - Dorf, Martin E
AU  - Dorf ME
LA  - eng
GR  - CA67416/CA/NCI NIH HHS/United States
GR  - NS37284/NS/NINDS NIH HHS/United States
GR  - RG2989B3/RG/CSR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Glia
JT  - Glia
JID - 8806785
RN  - 0 (Ccl11 protein, mouse)
RN  - 0 (Chemokine CCL11)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CC)
RN  - 0 (Cytokines)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Virulence Factors, Bordetella)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 2.4.2.31 (Pertussis Toxin)
SB  - IM
MH  - Animals
MH  - Astrocytes/immunology/*metabolism/*pathology
MH  - Cells, Cultured
MH  - Chemokine CCL11
MH  - Chemokine CCL5/biosynthesis/*pharmacology
MH  - Chemokines/biosynthesis/pharmacology
MH  - Chemokines, CC/pharmacology
MH  - Cytokines/biosynthesis/pharmacology
MH  - Inflammation/genetics/immunology/metabolism
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Pertussis Toxin
MH  - Receptors, Chemokine/deficiency/*metabolism
MH  - Signal Transduction/*immunology
MH  - Virulence Factors, Bordetella/pharmacology
EDAT- 2002/07/12 10:00
MHDA- 2002/08/24 10:01
CRDT- 2002/07/12 10:00
PHST- 2002/07/12 10:00 [pubmed]
PHST- 2002/08/24 10:01 [medline]
PHST- 2002/07/12 10:00 [entrez]
AID - 10.1002/glia.10079 [doi]
PST - ppublish
SO  - Glia. 2002 Jul;39(1):19-30. doi: 10.1002/glia.10079.