Tumor necrosis factor alpha and transforming growth factor beta upregulate astrocyte expression of monocyte chemoattractant protein-1.
J Neuroimmunol
; 57(1-2): 193-8, 1995 Mar.
Article
in En
| MEDLINE
| ID: mdl-7706436
ABSTRACT
Astrocytes participate in the pathophysiology of central nervous system (CNS) inflammatory disease. Astrocyte expression of adhesion molecules, cytokines, and major histocompatibility complex antigens may contribute to these inflammatory processes. In addition, recent data suggested that astrocytes may be a source of monocyte chemoattractant protein-1 (MCP-1). MCP-1 is a member of the chemokine family of small cytokines and functions both as a chemoattractant as well as a stimulator of monocytes. To further characterize the role of astrocytes in CNS inflammation, we examined the effect of inflammatory cytokines on MCP-1 expression by astrocytes. Results of these studies demonstrate that the pro-inflammatory cytokine tumor necrosis factor alpha (TNF alpha) upregulates MCP-1 message and protein expression. The pleiotropic cytokine transforming growth factor beta (TGF beta) also stimulated MCP-1 expression. When astrocytes were exposed to both cytokines simultaneously, an additive effect on MCP-1 message, but not MCP-1 protein expression, was observed. These data suggest that TNF alpha and TGF beta, each present during CNS inflammatory disease, may upregulate the expression of MCP-1 which, in turn, may function to both recruit monocytes to the site of inflammation as well as to activate those monocytes already present in an inflammatory lesion.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Chemotactic Factors
/
Gene Expression Regulation
/
Astrocytes
/
Transforming Growth Factor beta
/
Tumor Necrosis Factor-alpha
Limits:
Humans
Language:
En
Journal:
J Neuroimmunol
Year:
1995
Document type:
Article
Affiliation country:
United States