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Peroxynitrite induces covalent dimerization of epidermal growth factor receptors in A431 epidermoid carcinoma cells
A van der Vliet1, M Hristova, C E Cross
1Center for Comparative Respiratory Biology and Medicine, Department of Internal Medicine, University of California, Davis, California 95616, USA.
Abstract:
Irreversible tyrosine modifications by inflammatory oxidants such as peroxynitrite (ONOO-) can affect signal transduction pathways involving tyrosine phosphorylation. The epidermal growth factor receptor (EGFR), a member of the c-ErbB receptor tyrosine kinase family, is involved in regulation of epithelial cell growth and differentiation, and possible modulation of EGFR-dependent signaling by ONOO- was studied. Exposure of epidermoid carcinoma A431 cells to 0.1-1.0 mM ONOO- resulted in tyrosine nitration on EGFR and other proteins but did not significantly affect EGFR tyrosine autophosphorylation. A high molecular mass tyrosine-phosphorylated protein (approximately 340 kDa) was detected in A431 cell lysates after exposure to ONOO-, most likely representing a covalently dimerized form of EGFR, based on immunoprecipitation and/or immunoblotting with alpha-EGFR antibodies and co-migration with ligand-induced EGFR dimers cross-linked with 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide. Covalent EGFR dimerization by ONOO- probably involved intermolecular dityrosine cross-linking and was enhanced after receptor activation with epidermal growth factor. Furthermore, irreversibly cross-linked EGFR was more extensively tyrosine-phosphorylated compared with the monomeric form, indicating that ONOO- preferentially cross-links activated EGFR. Exposure of A431 cells to ONOO- markedly reduced the kinetics of tyrosine phosphorylation of a downstream EGFR substrate, phospholipase C-gamma1, which may be related to covalent alterations in EGFR. Alteration of EGFR signaling by covalent EGFR dimerization by inflammatory oxidants such as ONOO- may affect conditions of increased EGFR activation such as epithelial repair or tumorigenesis.
Insights
Inflammatory oxidants like peroxynitrite (ONOO-) can cause irreversible tyrosine modifications. This study shows ONOO- covalently dimerizes epidermal growth factor receptor (EGFR), altering its signaling and downstream effects.
Area of Science:
- Biochemistry
- Cell Signaling
- Oxidative Stress
Background:
- Tyrosine phosphorylation is crucial for signal transduction.
- Inflammatory oxidants, such as peroxynitrite (ONOO-), can modify tyrosine residues.
- Epidermal Growth Factor Receptor (EGFR) signaling regulates cell growth and differentiation.
Purpose of the Study:
- To investigate the modulation of EGFR-dependent signaling by ONOO-.
- To determine if ONOO- affects EGFR tyrosine phosphorylation and dimerization.
- To understand the consequences of ONOO- induced EGFR alterations on downstream signaling.
Main Methods:
- Exposure of A431 epidermoid carcinoma cells to ONOO-.
- Analysis of tyrosine nitration and phosphorylation on EGFR and other proteins.
- Immunoprecipitation and immunoblotting with anti-EGFR antibodies.
- Cross-linking of EGFR dimers using 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC).
Main Results:
- ONOO- induced tyrosine nitration on EGFR but did not significantly affect its autophosphorylation.
- A 340 kDa tyrosine-phosphorylated protein, identified as covalently dimerized EGFR, was detected.
- ONOO- enhanced covalent EGFR dimerization, particularly after epidermal growth factor activation.
- Irreversibly cross-linked EGFR showed increased tyrosine phosphorylation.
- ONOO- reduced the tyrosine phosphorylation kinetics of phospholipase C-gamma1, a downstream EGFR substrate.
Conclusions:
- ONOO- induces covalent dimerization of EGFR, likely through dityrosine cross-linking.
- This covalent dimerization preferentially occurs with activated EGFR.
- ONOO--mediated EGFR dimerization alters downstream signaling, potentially impacting epithelial repair and tumorigenesis.