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  • Title: [An exploratory study on mechanism of PPARalpha activators-induced plasminogen activator inhibitor-1 expression in HepG-2 cells].
    Author: Ye P, He YL, Wang Q, Liu YX.
    Journal: Zhonghua Nei Ke Za Zhi; 2004 Oct; 43(10):743-6. PubMed ID: 15631825.
    Abstract:
    OBJECTIVE: To investigate the influence of peroxisome proliferator-activated receptor alpha activators on plasminogen activator inhibitor-1 (PAI-1) expression in HepG-2 cells and the mechanism possibly involved. METHODS: Linoleic acid and fenofibrate were used in the treatment of HepG-2 cell culture. PAI-1 activity and mRNA expression were determined with colorimetric assay and reverse transcription-polymerase chain reaction, respectively. Using gene recombination techniques, two types of chloramphenicol acetyl transferase (CAT) reporter gene plasmid containing different deletions in PAI-1 promoter were constructed and transiently transfected into HepG-2 cells, respectively. Linoleic acid and fenofibrate were added to induce the transfected cells. CAT activity was measured to demonstrate the transcriptional activity of PAI-1 gene in HepG-2 cells. RESULTS: The mRNA expression and protein activity of PAI-1 was significantly induced by linoleic acid, but was obviously suppressed by fenofibrate. In the HepG-2 cells transfected with PAI-pCAT promoter constructs the PAI-1 transcription activity was significantly induced by linoleic acid, but suppressed by fenofibrate. The level of PAI-1 transcription was also significantly increased when co-transfected with PAI-pCAT promoter construct and PPAR alpha-pSG5 expression plasmid to HepG-2 cells. Furthermore, in the condition of transfection with NF-kappaB-response element-deletion-pCAT construct, both linoleic acid and fenofibrate increased the PAI-1 transcriptional activity, whereas in those cells transfected with VLDL/fatty acid response element-deletion-pCAT construct, fenofibrate significantly reduced PAI-1 transcriptional activity, but no change in PAI-1 transcription activity was found with linoleic acid stimulation. CONCLUSIONS: Linoleic acid induces PAI-1 activity and mRNA expression in HepG-2 cells. PPAR alpha may be one of transcription factors playing a role in the upregulation of PAI-1 gene expression. The inhibition of NF-kappaB signaling pathway may be involved in the downregulation of PAI-1 gene expression by fenofibrate.
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