Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

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.

Annotation

Gene Ontology Annotations
Objects Annotated

Additional Information

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



NHLBI Logo

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