PMID- 8300851
OWN - NLM
STAT- MEDLINE
DCOM- 19940308
LR  - 20190825
IS  - 0165-5728 (Print)
IS  - 0165-5728 (Linking)
VI  - 50
IP  - 1
DP  - 1994 Feb
TI  - Regulation of monocyte chemoattractant protein-1 expression in adult human 
      non-neoplastic astrocytes is sensitive to tumor necrosis factor (TNF) or antibody 
      to the 55-kDa TNF receptor.
PG  - 101-7
AB  - Infiltration of the central nervous system (CNS) by monocytes is a characteristic 
      of many non-malignant disease processes, although the signals regulating such 
      traffic are unclear. Tumor necrosis factor (TNF) and other inflammatory cytokines 
      have been shown to elicit production of monocyte chemoattractant activity in 
      glioma cells, but the regulation of such activity in non-neoplastic adult 
      astrocytes has not been examined. We previously observed that TNF constituted a 
      proliferative signal for non-neoplastic adult human astrocytes in vitro involving 
      the 55-kDa TNF receptor. In the present study, we demonstrate that TNF exposure 
      enhances the expression of monocyte chemoattractant protein-1 (MCP-1) mRNA and 
      functional monocyte chemoattractant activity in non-neoplastic astrocytes. 
      Results indicated that MCP-1 mRNA expression was maximal within 3 h, and was 
      further augmented by the protein synthesis inhibitor cycloheximide (CY). Antibody 
      (htr-9) directed against the 55-kDa TNF receptor also elicited MCP-1 mRNA 
      expression while antibody to the 75-kDa TNF receptor (utr-1) was ineffective. 
      Secretion of monocyte chemoattractant activity was significantly greater in TNF- 
      or htr-9-treated astrocytes than in utr-1-treated or untreated controls; activity 
      was abolished by treatment with antibody to MCP-1. These findings suggest that 
      non-neoplastic adult human astrocytes may contribute to CNS inflammatory 
      responses by mediating recruitment of peripheral blood monocytes.
FAU - Barna, B P
AU  - Barna BP
AD  - Department of Clinical Pathology, Cleveland Clinic Foundation, OH 44195-5131.
FAU - Pettay, J
AU  - Pettay J
FAU - Barnett, G H
AU  - Barnett GH
FAU - Zhou, P
AU  - Zhou P
FAU - Iwasaki, K
AU  - Iwasaki K
FAU - Estes, M L
AU  - Estes ML
LA  - eng
GR  - 1454-HL/HL/NHLBI NIH HHS/United States
GR  - NCI-R01 CA49950/CA/NCI 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  - Netherlands
TA  - J Neuroimmunol
JT  - Journal of neuroimmunology
JID - 8109498
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antibodies, Monoclonal/*immunology
MH  - Astrocytes/drug effects/*metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*biosynthesis/genetics
MH  - Cytokines/*biosynthesis
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - RNA, Messenger/analysis
MH  - Receptors, Tumor Necrosis Factor/*physiology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1994/02/01 00:00
MHDA- 2000/06/01 09:00
CRDT- 1994/02/01 00:00
PHST- 1994/02/01 00:00 [pubmed]
PHST- 2000/06/01 09:00 [medline]
PHST- 1994/02/01 00:00 [entrez]
AID - 0165-5728(94)90220-8 [pii]
AID - 10.1016/0165-5728(94)90220-8 [doi]
PST - ppublish
SO  - J Neuroimmunol. 1994 Feb;50(1):101-7. doi: 10.1016/0165-5728(94)90220-8.