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Regulation of plasminogen activator inhibitor-1 mRNA accumulation by basic fibroblast growth factor and transforming growth factor-beta1 in cultured rat astrocytes.

Authors: Treichel, JA  Reddington, M  Kreutzberg, GW 
Citation: Treichel JA, etal., J Neurochem. 1998 Nov;71(5):1944-52.
Pubmed: (View Article at PubMed) PMID:9798919

The effects of transforming growth factor-beta1 (TGF-beta1) and basic fibroblast growth factor (bFGF) were examined on the accumulation of plasminogen activator inhibitor-1 (PAI-1) mRNA in astrocytes in vitro. Both cytokines stimulated PAI-1 mRNA expression transiently with a maximal fivefold (bFGF) and 30-fold (TGF-beta1) at 4 h, decreasing to basal levels within 32 h. EC50 values were 1.4 nM for bFGF and 6.7 pM for TGF-beta1 on PAI-1 mRNA accumulation. A twofold increase in content of tPA mRNA was observed with bFGF but not with TGF-beta1. The action of TGF-beta1 on PAI-1 mRNA was inhibited by cycloheximide, indicating a requirement for de novo protein synthesis. In contrast, cycloheximide potentiated the action of bFGF. Nuclear run-on assays showed that bFGF, but not TGF-beta1, stimulated astrocytic PAI-1 gene transcription. Thus, TGF-beta1 predominantly uses posttranscriptional mechanisms to raise the level of PAI-1 mRNA in astrocytes, whereas bFGF acts at both the transcriptional and posttranscriptional levels. The data reveal differences in the mechanisms underlying the regulation of PAI-1 mRNA levels by TGF-beta1 in astrocytes compared with other cells. The action of TGF-beta1 and bFGF on the plasminogen activator system in astrocytes might be involved in the cellular events accompanying glial activation following injury of the CNS.


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CRRD Object Information
CRRD ID: 8547916
Created: 2014-02-28
Species: All species
Last Modified: 2014-02-28
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.