Nucleic Acids Research, 1991, Vol. 19, No. 1 163-168
© 1991
MOLECULAR BIOLOGY |
Transcriptional regulation of plasminogen activator inhibitor type-1 mRNA in Hep G2 cells by epidermal growth factor
Department of Medicine, Washington University School of Medicine St Louis, MO 63110, USA
*To whom correspondence should be addressed at Cardiovascular Division, Box 8086, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
Received June 12, 1990. Revised November 29, 1990. Accepted November 29, 1990.
Secretion of plasminogen activator inhibitor type-1 (PAI-1) by cultured cells Is increased after exposure to specific cytoklnes and growth factors. We have shown previously that incubation of Hep G2 cells with epidermal growth factor (EGF) results in a marked increase in steady state levels of PAI-1 mRNA (Lucore, C.L., et al. (1988) J. Blol. Chem. 263, 15845–15848). The present study was undertaken to determine whether the regulation of expression of PAI-1 mRNA by EGF is mediated at the level of transcription and/or by post- transcriptional mechanisms. The rate of transcription of the PAI-1 gene measured by nuclear run-on assays was found to be increased within 2 h after stimulation of the cells with EGF (5 ng/ml) (3.2 fold Increase relative to control, n = 2, range 3.0–3.4). It reached a maximum in 3 h, (9.2 fold increase relative to control, n = 2, range 8.8–9.6) and returned to baseline in 5 h. Exposure of the cells to EGF did not Increase the rate of transcription of the glyceralde-hyde-3-phosphate dehydrogenase gene. The half life of PAI-1 mRNA in Hep G2 cells was 120 min as determined by RNA blot analysis after exposure of the cells to actinomycin D to inhibit transcription. Stimulation of the cells with EGF did not result in significant change in the half life of PAI-1 mRNA. The results demonstrate that exposure of Hep G2 cells to EGF increases PAI-1 gene transcription.
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