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IRES-dependent regulation of FGF-2 mRNA translation in pathophysiological conditions in the mouse

I G Gonzalez-Herrera1, L Prado-Lourenco, S Teshima-Kondo

  • 1Institut National de la Santé et de la Recherche Médicale U589, "Hormones, facteurs de croissance et physiopathologie vasculaire", Institut Louis Bugnard, IFR31, CHU Rangueil, Bâtiment L3, Avenue Jean Poulhès, BP 84225, 31432 Toulouse Cedex 4, France.

Biochemical Society Transactions
|October 26, 2005
PubMed

Insights

Fibroblast growth factor 2 (FGF-2) expression is regulated by an internal ribosome entry site (IRES). This study reveals FGF-2 IRES activation in the aorta under diabetic conditions, contributing to atherosclerosis.

Area of Science:

  • Molecular Biology
  • Genetics
  • Physiology

Background:

  • Fibroblast growth factor 2 (FGF-2) is a key angiogenic factor whose mRNA translation relies on an internal ribosome entry site (IRES).
  • Understanding FGF-2 regulation is crucial, particularly in pathophysiological contexts like diabetes, which involves vascular complications.

Purpose of the Study:

  • To investigate the role of the FGF-2 IRES in regulating FGF-2 expression in vivo under both normal and pathophysiological conditions.
  • To explore the translational control of FGF-2 mRNA in diabetic hyperglycemia and its implications for atherosclerosis.

Main Methods:

  • Generation of transgenic mice lines expressing bioluminescent bicistronic transgenes to analyze FGF-2 IRES activity.
  • In vivo studies in streptozotocin-induced diabetic mice to assess FGF-2 IRES activation in the aorta wall.

Main Results:

  • FGF-2 IRES activity exhibits significant tissue specificity in adult brain and testis.
  • Diabetic hyperglycemia specifically activates the FGF-2 IRES in the aorta wall, correlating with increased endogenous FGF-2 expression.
  • IRES activation contributes to FGF-2 overexpression when cap-dependent translation is impaired under hyperglycemic conditions.

Conclusions:

  • The FGF-2 IRES plays a critical role in regulating FGF-2 expression, with tissue-specific activity in the brain and testis.
  • FGF-2 IRES activation under hyperglycemic conditions contributes to FGF-2 overexpression and exacerbates diabetes-linked atherosclerosis.
  • IRES trans-acting factors (ITAFs) like p53 and hnRNP AI may modulate FGF-2 IRES activity in pathophysiological states.

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