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Heparin protects basic and acidic FGF from inactivation.

D Gospodarowicz, J Cheng

    Journal of Cellular Physiology
    |September 1, 1986
    PubMed
    Summary
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    Heparin and hexuronyl hexosaminoglycan sulfate (HHS-4) protect fibroblast growth factors (FGF) from inactivation by acid or heat. These compounds also potentiate FGF bioactivity, suggesting a dual protective and potentiating role.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Molecular Biology

    Background:

    • Basic and acidic fibroblast growth factors (FGF) are crucial mitogens for cell growth.
    • FGF potency can be affected by storage conditions and environmental factors like pH and temperature.
    • Heparin and hexuronyl hexosaminoglycan sulfate (HHS-4) are known to interact with growth factors.

    Purpose of the Study:

    • To analyze the protective ability of heparin and HHS-4 against FGF inactivation.
    • To investigate the potentiating effects of heparin and HHS-4 on FGF bioactivity.
    • To understand the mechanism of action of heparin and HHS-4 on FGF.

    Main Methods:

    • Assessing the mitogenic activity of basic and acidic FGF on baby hamster kidney (BHK-21) cells.
    • Exposing FGF to acidic (1% trifluoroacetic acid) or heat (65°C) conditions with and without heparin or HHS-4.

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  • Measuring the retained potency of FGF after inactivation treatments in the presence of heparin or HHS-4.

    • Main Results:

    • Freshly prepared basic FGF was 10-fold more potent than acidic FGF.
    • Heparin decreased basic FGF potency but potentiated acidic FGF potency.
    • Heparin and HHS-4 protected both basic and acidic FGF from acid and heat inactivation, preserving their potency.
    • Heparin and HHS-4 also potentiated the bioactivity of protected or inactivated FGF at high concentrations.

    Conclusions:

    • Heparin and HHS-4 exhibit a protective effect on FGF against inactivation.
    • These glycosaminoglycans also potentiate FGF bioactivity, indicating a dual role.
    • An additional, unidentified locus of action for heparin and HHS-4 in potentiating FGF activity is suggested.