Staphylococcus aureus alpha-toxin. 2. Reduction of epidermal growth factor receptor affinity in PC12 cells.

Abstract

Staphylococcus aureus alpha-toxin, at sub-cytotoxic concentrations, inhibits both the 125I-labeled epidermal growth factor (EGF) binding and autophosphorylation properties of EGF-receptors in PC12 cells. This inhibition occurred only in intact cells and is probably due to a decrease in the affinity of the receptor for EGF. Streptolysin S and parcelsin could mimic the alpha-toxin effect below cytotoxic concentrations, as measured by a 51Cr release assay. In contrast, other membrane perturbing toxins with different lipid specificity, such as tetanolysin and cobra direct lytic factor, inhibited [125I]EGF binding only at cytotoxic concentrations. Staphylococcal alpha-toxin also stimulated 3-fold the specific binding of a radioactive tumor-promoting phorbol ester (PDBu) to PC12 cells at concentrations similar to those required for the inhibition of [125I]EGF binding. Although the exact mechanism for the inhibition of EGF binding by alpha-toxin has not been established, our results suggest that protein kinase C may be involved in this time-dependent process.

• Authors: P Lazarovici, K F Chan
• Journal: Toxicon : official journal of the International Society on Toxinology (Toxicon) Vol. 25 Issue 6 Pg. 637-47 ( 1987) ISSN: 0041-0101 [Print] England
• PMID: 3498239 (Publication Type: Journal Article)

Chemical References

• Bacterial Toxins
• Cross-Linking Reagents
• Hemolysin Proteins
• Iodine Radioisotopes
• staphylococcal alpha-toxin
• Epidermal Growth Factor
• ErbB Receptors
• Protein-Tyrosine Kinases
• Protein Kinase C

Topics

• Animals
• Bacterial Toxins (pharmacology)
• Cell Membrane (drug effects, metabolism)
• Cell Survival (drug effects)
• Cells, Cultured
• Cross-Linking Reagents
• Epidermal Growth Factor (metabolism)
• ErbB Receptors (metabolism)
• Hemolysin Proteins
• Iodine Radioisotopes
• Membrane Potentials (drug effects)
• Protein Kinase C (metabolism)
• Protein-Tyrosine Kinases (metabolism)