Basal expression and insulin-mediated induction of PAI-1 mRNA in Hep G2 cells

P. J. Grant, M. Rüegg, R. L. Medcalf

Research output: Contribution to journalArticleResearchpeer-review

16 Citations (Scopus)

Abstract

We have explored the effect of insulin on the modulation of mRNA and antigen levels of components of the fibrinolytic enzyme system in human hepatoma (Hep G2) and fibrosarcoma (HT-1080) cells. Treatment of Hep G2 cells with a physiological concentration of insulin provokes a 2-fold increase in plasminogen activator inhibitor (PAI)-1 antigen. A similar increase is observed for both the 3.2 and 2.3 kb transcripts of PAI-1 mRNA. Cycloheximide when added alone to cells preferentially suppresses constitutive expression of the 3.2 kb PAI-1 mRNA and blocks insulin-mediated induction of both 3.2 and 2.3kb PAI-1 mRNA. There was no detectable expression of urokinase (u-PA) or tissue-type plasminogen activator (t-PA) antigen or mRNA in these cells under constitutive conditions or after treatment with insulin. In HT-1080 cells, basal expression of PAI-1, t-PA and u-PA mRNA and antigen was not modulated by insulin treatment. The results from these experiments indicate firstly, that induction of PAI-1 by insulin requires on-going protein biosynthesis, and secondly, that the two species of PAI-1 mRNA have a different requirement for protein biosynthesis.

Original languageEnglish
Pages (from-to)81-86
Number of pages6
JournalFibrinolysis and Proteolysis
Volume5
Issue number2
DOIs
Publication statusPublished - 1 Jan 1991
Externally publishedYes

Keywords

  • Cycloheximide
  • Insulin
  • Plasminogen activator inhibitor 1

Cite this

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abstract = "We have explored the effect of insulin on the modulation of mRNA and antigen levels of components of the fibrinolytic enzyme system in human hepatoma (Hep G2) and fibrosarcoma (HT-1080) cells. Treatment of Hep G2 cells with a physiological concentration of insulin provokes a 2-fold increase in plasminogen activator inhibitor (PAI)-1 antigen. A similar increase is observed for both the 3.2 and 2.3 kb transcripts of PAI-1 mRNA. Cycloheximide when added alone to cells preferentially suppresses constitutive expression of the 3.2 kb PAI-1 mRNA and blocks insulin-mediated induction of both 3.2 and 2.3kb PAI-1 mRNA. There was no detectable expression of urokinase (u-PA) or tissue-type plasminogen activator (t-PA) antigen or mRNA in these cells under constitutive conditions or after treatment with insulin. In HT-1080 cells, basal expression of PAI-1, t-PA and u-PA mRNA and antigen was not modulated by insulin treatment. The results from these experiments indicate firstly, that induction of PAI-1 by insulin requires on-going protein biosynthesis, and secondly, that the two species of PAI-1 mRNA have a different requirement for protein biosynthesis.",
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Basal expression and insulin-mediated induction of PAI-1 mRNA in Hep G2 cells. / Grant, P. J.; Rüegg, M.; Medcalf, R. L.

In: Fibrinolysis and Proteolysis, Vol. 5, No. 2, 01.01.1991, p. 81-86.

Research output: Contribution to journalArticleResearchpeer-review

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N2 - We have explored the effect of insulin on the modulation of mRNA and antigen levels of components of the fibrinolytic enzyme system in human hepatoma (Hep G2) and fibrosarcoma (HT-1080) cells. Treatment of Hep G2 cells with a physiological concentration of insulin provokes a 2-fold increase in plasminogen activator inhibitor (PAI)-1 antigen. A similar increase is observed for both the 3.2 and 2.3 kb transcripts of PAI-1 mRNA. Cycloheximide when added alone to cells preferentially suppresses constitutive expression of the 3.2 kb PAI-1 mRNA and blocks insulin-mediated induction of both 3.2 and 2.3kb PAI-1 mRNA. There was no detectable expression of urokinase (u-PA) or tissue-type plasminogen activator (t-PA) antigen or mRNA in these cells under constitutive conditions or after treatment with insulin. In HT-1080 cells, basal expression of PAI-1, t-PA and u-PA mRNA and antigen was not modulated by insulin treatment. The results from these experiments indicate firstly, that induction of PAI-1 by insulin requires on-going protein biosynthesis, and secondly, that the two species of PAI-1 mRNA have a different requirement for protein biosynthesis.

AB - We have explored the effect of insulin on the modulation of mRNA and antigen levels of components of the fibrinolytic enzyme system in human hepatoma (Hep G2) and fibrosarcoma (HT-1080) cells. Treatment of Hep G2 cells with a physiological concentration of insulin provokes a 2-fold increase in plasminogen activator inhibitor (PAI)-1 antigen. A similar increase is observed for both the 3.2 and 2.3 kb transcripts of PAI-1 mRNA. Cycloheximide when added alone to cells preferentially suppresses constitutive expression of the 3.2 kb PAI-1 mRNA and blocks insulin-mediated induction of both 3.2 and 2.3kb PAI-1 mRNA. There was no detectable expression of urokinase (u-PA) or tissue-type plasminogen activator (t-PA) antigen or mRNA in these cells under constitutive conditions or after treatment with insulin. In HT-1080 cells, basal expression of PAI-1, t-PA and u-PA mRNA and antigen was not modulated by insulin treatment. The results from these experiments indicate firstly, that induction of PAI-1 by insulin requires on-going protein biosynthesis, and secondly, that the two species of PAI-1 mRNA have a different requirement for protein biosynthesis.

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